It’s time to make a plan for nuclear waste

Today, nuclear energy enjoys a rare moment of support across the political spectrum in the US. Interest from tech companies that are scrambling to meet demand for massive data centers has sparked a resurgence of money and attention in the industry. That newfound interest is exactly why it’s time to talk about an old problem: nuclear waste. 

In the US alone, nuclear reactors produce about 2,000 metric tons of high-level waste each year. And there’s nowhere to put it.

Though newly popular, the nuclear program in the US is nothing new. The US hosts more reactors and production capacity than any other country in the world. And yet nearly seven decades after the first permanent nuclear facility in the US went online, there’s still not a long-term solution for nuclear waste. 

Used fuel is largely stored onsite at operating and shut-down reactors, in pools and casks made of steel and concrete. Experts generally agree that these methods are safe, but they’re not designed to be permanent.

The leading strategy around the world for long-term storage of this high-level radioactive waste is to house it in a deep geological repository—dig a hole, put radioactive material down there, and fill it up with concrete. These holes, hundreds of meters underground, are designed to be a permanent home.

There aren’t any operating geological repositories for spent fuel yet, but some countries are well on their way. Finland is the furthest along; as of 2026, the country is testing its facility. Final approvals are expected soon, and operations could start later this year. Some other countries aren’t far behind.

France is home to over 50 nuclear reactors, and its grid gets more of its power from nuclear than any other. The country also has the world’s most established program for reprocessing spent fuel. The process separates out the plutonium and uranium to create a type of fuel known as mixed oxide (MOX) fuel. But reprocessing isn’t a perfect recycling loop, so the leftovers from this process still need somewhere to go. The country currently stores waste onsite at the La Hague reprocessing plant, but it plans to build a repository. Initial approvals could come later this decade, and pilot operations could start up by 2035.

Technically, the US also has a destination for its spent fuel: Yucca Mountain in Nevada. The site, which is on federal land, was designated by Congress in 1987. However, progress has entirely stalled out because of political opposition. In 2011, the federal government stopped providing funding for the site, and for roughly a decade, there’s been no activity to speak of.

In the meantime, waste continues to pile up.

The nuclear industry is kicking into a new gear around the world. China is home to the world’s fastest–growing nuclear energy program, and countries including Bangladesh and Turkey are building their first reactors.

Even the long-established US program is seeing growth: Interest in and approval for nuclear energy have spiked, and Big Tech is throwing money around to meet rising electricity demand. Companies are proposing (and beginning to receive regulatory approval for) next-generation reactors, which employ different coolants, fuels, and designs.

Given all this new interest, and the impending arrival of new types of nuclear waste, it’s time for nuclear companies, as well as their powerful customers, to push for progress on building geological storage facilities. As the richest country on the planet and home to a large chunk of the activity in next-generation reactors, the US should aim to join the leaders rather than continue to lag behind. 

Directing even a small fraction of the recent surge in funding and attention to progress on waste could make a difference. Some experts are calling for a new organization in the US to manage nuclear waste rather than leaving it to the Department of Energy. This organization would mirror programs in Finland, Canada, and France.

The process of planning, building, and commissioning a permanent solution for nuclear waste is a long one. Finland started planning in the 1980s and selected its site in the early 2000s, and it’s nearly ready to start accepting waste. For countries that don’t have a permanent storage solution sorted, the best time to start was decades ago. But the second-best time is now. 

This article is from The Spark, MIT Technology Review’s weekly climate newsletter. To receive it in your inbox every Wednesday, sign up here

One Biosciences Chooses Albany, NY, as Its U.S. Location

Paris-based One Biosciences, an Institut Curie-backed startup, plans to set up, staff, and equip a high-complexity lab and computational analytics operation in Albany, NY, as its first U.S. location.

Empire State Development is supporting this expansion with up to $525,000 in performance-based Excelsior Jobs Program tax credits in exchange for the company’s job commitments, which anticipate 42 life science jobs and $18 million in investments over the next five years.

Officials at One Biosciences say the company will bring its proprietary technology to the first-of-its-kind hub in Albany to address the unmet clinical and scientific needs to characterize the tumor ecosystem by means of a single-cell profiling approach.

We are excited to accelerate support of our pharma, biotech, and academic collaborators through our AI-driven single-cell technologies, which will ultimately benefit physicians and their patients,” added Vincent Miller, MD, executive chairman, One Biosciences. “The local Albany life sciences ecosystem gives us access to a community of like-minded researchers and physicians committed to leveraging technology to improve health and is an ideal location from where to serve the U.S. globally.”

“Life science research and development is vital to creating the treatments that help people heal, survive and live longer,” said New York governor Kathy Hochul. “Through our targeted efforts, we are working to ensure that cutting edge companies like One Biosciences not only grow here, but that the next generation of medical breakthroughs happen in New York State.”

The post One Biosciences Chooses Albany, NY, as Its U.S. Location appeared first on GEN – Genetic Engineering and Biotechnology News.

Impact of extremely low frequency electromagnetic fields exposure on sleep quality and mental health in a Tunisian power plant: a cross-sectional study

IntroductionExtremely low-frequency electromagnetic fields (ELF-EMFs) are ubiquitous in our daily life. They may have an impact not only on physical health but also on mental health.ObjectivesTo assess the impact of occupational exposure to the ELF-EMFs on sleep quality, depression, anxiety and stress among workers at the Tunisian Electricity and Gas Company (TEGC).MethodsThis was a cross-sectional study. The study population included two groups: an exposed group (EG), consisting of power plant employees, and a non-exposed group (NEG), consisting of administrative workers. Exposure to ELF-EMFs was assessed via spot measurements using a magnetometer. Sleep quality, depression, anxiety and stress were assessed by the French versions of the Pittsburgh Sleep Quality Index (PSQI) and the Depression, Anxiety and Stress Scale (DASS-21).ResultsSeventy-seven participants in the EG and 88 participants in the NEG were included in the study. The median value of the ELF-EMFs was 5.86 μT at the power plant [min 0.1, max 40.34 μT]. According to the PSQI global score, 64.9% of the EG had poor sleep quality versus 29.5% of the NEG. Depression was registered in 24.7% of EG and in 3.4% of NEG. Anxiety was noted in 23.4% of the EG and in none of the NEG. Stress was found in 46.8% of the EG and none of the NEG. After multivariate analysis, ELF-EMF exposure was significantly associated with poor sleep quality and depression.ConclusionThe present study revealed that ELF-EMFs can affect sleep and mental health. Further studies are needed to explain the mechanism involved.

Cyclothymic and anxious affective temperament in perinatal depression: findings from an exploratory cross-sectional study

IntroductionThe perinatal period represents a vulnerable period in which women may experience high psychic distress due to psychological, biological and social changes. The prevalence of perinatal depression (PND) is estimated around 15%-20% during pregnancy and 16%-18% after childbirth. Although several risk factors have been investigated in the PND development, few studies explored the role of affective temperaments, well known to exert a role in any mood disorders. The aim of our study was to explore which is the most represented affective temperamental profile in PND as well as which is its role in the development and severity of depressive symptoms during perinatal period.MethodsAll pregnant women admitted at the Perinatal Mental Health Outpatient Service, Unit of Clinical Psychiatry, University Hospital of Marche, Polytechnic University of Marche, Ancona, Italy, between April 2021 and July 2025, were screened for PND through Edinburgh Postnatal Depression Scale (EPDS) and a semi-structured clinical interview (SCID-5-CV). Temperament Evaluation of Memphis, Pisa, Paris and San Diego (TEMPS-M) was administered to all pregnant women. ResultsThe PND prevalence was 33.1%. PND was significantly associated with higher cyclothymic (B = 0.356, p = 0.001) and anxious TEMPS-M scores (B = 0.247, p = 0.026) and a positive psychiatric history (B = 5.245, p < 0.001) (R = 0.6, R2 = 0.36, F(3,129) = 24.189, p < 0.001). Logistic regression indicated that cyclothymic (Exp(B)=1.118, p=0.008), hyperthymic (Exp(B)=0.911, p=0.049), anxious temperaments (Exp(B)=1.109, p=0.029), presence of medical comorbidities (Exp(B)=0.224, p=0.003) and psychiatric history (Exp(B)=5.144, p=0.001) were independent predictors of PND.DiscussionAffective temperaments, particularly cyclothymic and anxious profiles, and prior psychiatric history are predictors of perinatal depression. Incorporating temperament assessment alongside standard screening tools such as the EPDS may improve early identification of women at risk, supporting tailored preventive and therapeutic strategies.

Hearing Loss Gene Therapy Lasts More than Two Years

A trial of a gene therapy to treat people with hearing loss related to recessive mutations in the OTOF gene shows the treatment is effective and safe for at least 2.5 years.

The study, published in Nature, showed around 90% of those who received the adeno-associated viral (AAV) vector gene therapy showed at least some restoration in hearing.

Improvement was rapid in the first six weeks, improved further by 26 weeks and in a small subset of patients remained stable for 2.5 years of follow-up.

“It’s remarkable to see patients go from complete deafness to being able to hear,” said the study’s co-lead author, Zheng-Yi Chen, PhD, the Ines and Fredrick Yeatts Chair in Otolaryngology and an associate scientist at Massachusetts Eye and Ear hospital, in a press statement. “For many patients, that also means the ability to develop and use speech.”

The OTOF gene encodes the otoferlin protein, which is critical for normal hearing. When otoferlin is missing or nonfunctional, inner‑ear hair cells can’t relay sound information to the brain, leading to severe or complete deafness. This kind of hearing loss is rare and inherited in a recessive manner, needing mutations from both parents for a child to be affected.

As of this year there are at least five gene therapies being developed to treat this kind of deafness, for example, by Akouos/Eli Lilly and Decibel/Regeneron in the U.S., Sensorion in France, and at least two additional programs in China.

The current study took place in China and included 42 people between the age of eight months and 32 years (average age six years) and is the largest cohort of OTOF gene‑therapy patients reported so far, as well as the longest study follow-up period.

The participants received one of three doses of the AAV gene therapy injected into their cochlea’s and were followed up for 13 weeks to 2.5 years (median 52 weeks) to assess the impact of the therapy on hearing and also to evaluate safety.

Overall no serious adverse events or dose-limiting toxicities occurred. Around 90% of participants experienced hearing restoration to some degree with fast improvements seen in the first six weeks after treatment and slower improvements after that. A subset of patients (seven ears from seven patients) were included in the 2.5 year follow-up group and results were similar to those seen at two years.

Some groups did better than others. For example, hearing restoration was 100% in children aged up to three years and 92% in those aged 3-8 years. Improvement was seen in older children and adults, but to a lesser degree than that seen in young children in the study. Participants with better outer hair cell function on enrollment also responded better to the therapy than those with greater functional loss.

“It is very encouraging to see meaningful improvements in some adult patients. It suggests there may be more flexibility in the human auditory system than we expected,” said Chen, who is also the scientific founder of Salubritas Therapeutics, a Massachusetts based biotech focusing on hearing loss correction.

The post Hearing Loss Gene Therapy Lasts More than Two Years appeared first on Inside Precision Medicine.

StockWatch: Revolution’s Phase III Pancreatic Cancer Data Dazzles Investors, Analysts

Pancreatic cancer is one of the most difficult cancers to treat, with an overall five-year survival rate of 13%, according to the American Cancer Society, stretching from 3% for metastatic (Stage 4) to 44% for localized (Stages 1 and 2).

Dismal odds such as these explain the enthusiastic response of investors when Revolution Medicine (NASDAQ: RVMD), a developer of RAS-addicted cancer therapies, announced dazzling data from its Phase III RASolute 302 trial (NCT06625320) evaluating its once-daily oral daraxonrasib in patients with metastatic pancreatic ductal adenocarcinoma (PDAC) who had been previously treated.

In the trial’s overall (intent-to-treat) study population, daraxonrasib showed a median overall survival (OS) of 13.2 months, nearly double the 6.7 months demonstrated for standard-of-care chemotherapy, with a hazard ratio (HR) of 0.40 (p < 0.0001). Daraxonrasib also presented what Revolution called a manageable safety profile and no new safety signals.

“These results represent a potentially transformative advance for patients and underscore daraxonrasib’s potential to redefine the treatment landscape. We are moving with urgency toward global regulatory submissions and remain committed to rapidly advancing this therapy for patients with a broad range of RAS-addicted cancers, Revolution’s CEO and chairman Mark A. Goldsmith, MD, PhD, said in a statement.

Investors and analysts largely agreed with Goldsmith. Revolution’s stock reacted to the data release by soaring 54% this past week, starting with a 41% surge that sent the share price soaring from $96.43 on April 10 to $136.30 on April 13. Since then, the stock has jumped another 12%, reaching $152.54 at Wednesday’s closing bell. Profit-taking by investors led to a 2% slide on Thursday (to $149.27) and a 0.43% dip on Friday (to $148.63).

“Our base case from stats sim [statistics simulation] was 11 vs. 7 mos, and based on our investor discussions, OS >12 months (and/or >6 mos delta vs. chemo) should drive meaningful stock upside,” Faisal Khurshid, an equity analyst with Jefferies, correctly predicted in an April 13 research note.

A “clear win” scenario, Khurshid explained, would show daraxonrasib with an OS of greater than 11 to 12 months, and/or a daraxonrasib difference vs. chemo of >4–6 months, and/or an HR of <0.5–0.6.

“Best-case outcome”

“The disclosed data materially exceeds these expectations,” Khurshid declared. “This is by any measure a best-case outcome for RVMD [emphasis in original]. Darax’s performance was roughly in line with the Ph1 experience, and chemo only slightly outperformed historical benchmarks.”

Revolution’s positive data sets the bar high for other cancer treatment developers—including Erasca (NASDAQ: ERAS), which is expected by the end of the first half to announce initial monotherapy data from its Phase I trial (NCT06983743) assessing ERAS-0015, a RAS-targeting molecule, in patients with RAS-mutant solid tumors.

Khurshid’s colleague at Jefferies, Maury Raycroft, PhD, noted Erasca has said it believes a >10% improvement in response rates in PDAC or non-small cell lung cancer compared to daraxonrasib could support ERAS-0015 as being differentiated from Revolution’s candidate, as would improvement in two or more safety/tolerability attributes, such as rash, gastrointestinal diseases, and stomatitis.

“Given the efficacy seen in ERAS’ 8 mg cohort and escalation to 40 mg, we remain (+)ve on the pot’l for stronger activity at higher doses,” Raycroft wrote in an April 13 research note. “That said, improved safety may be a key differentiator, particularly to enable combinations, especially as the competitive benchmark in PDAC continues to move higher.”

At Leerink Partners, Jonathan Chang, PhD, senior managing director, emerging oncology, and a senior research analyst, raised the firm’s 12-month share price target 28%, from $115 to $147, “to reflect greater conviction in pipeline opportunities.”

“Although RAS pathway drug development is highly competitive, we continue to believe encouraging clinical data from the innovative RAS(ON) platform, coupled with the large addressable population of RAS-dependent cancers, support a positive long-term outlook for RVMD,” Chang wrote.

Leerink colleague Andrew Berens, MD, senior managing director, targeted oncology, and a senior research analyst, observed that daraxonrasib could set a standard for positive data that several RAS-based cancer drug developers are working to improve upon, citing:

  • Adlai Nortye (NASDAQ: ANL): Its panRAS inhibitor AN9025 shares the same method of action as daraxonrasib but with potentially greater potency and durability. The company’s pipeline also includes AN4035, a panRAS antibody-drug conjugate.
  • BridgeBio Oncology Therapeutics (NASDAQ: BBOT): Its BBO-11818, a pan KRAS ON/OFF inhibitor, has shown efficacy signals in early PDAC clinical studies. “The more targeted ON/OFF approach may lead to greater potency and less toxicity.”
  • Immuneering (NASDAQ: IMRX): Its atebimetinib showed 64% OS at 12 months as a first-line pancreatic cancer treatment in updated data announced January 7.

“Not insurmountable”

“Dara[xonrasib] sets a high bar that is not insurmountable. The data for dara look encouraging, with a clear benefit over SOC [standard-of-care] chemo, but could leave room for other novel approaches to improve on efficacy and/or tolerability,” Berens wrote. “We think dara could be the first targeted therapy for RAS mutant PDAC patients and potentially become the 2L SOC, establishing RAS inhibitors as key backbone therapies in PDAC.”

That could lead to more RAS-based combination therapies, which Berens said has favorable implications for Tango Therapeutics (NASDAQ: TNGX)’s vopimetostat, an oral, selective PRMT5 inhibitor being studied in combinations with either daraxonrasib and another Revolution RAS(ON) cancer candidate, zoldonrasib, in a Phase I/II trial (NCT05732831).

Revolution said it plans to present its data at the American Society of Clinical Oncology’s 2026 ASCO Annual Meeting, set for May 29–June 2 in Chicago. Data will also be presented to regulators as Revolution files a New Drug Application (NDA) with the FDA, which has selected daraxonrasib for its Commissioner’s National Priority Voucher (CNPV).

Launched in October by FDA Commissioner Martin A. Makary, MD, CNPV is a pilot program that awards vouchers to drug developers whose work is deemed to address a health crisis in the United States, deliver more innovative cures, address unmet public health needs, and increase domestic drug manufacturing as a national security issue. In return, the vouchers entitle companies to reviews of their final applications within a target timeframe of 1–2 months rather than the current 10–12 months.

The stock surge boosted Revolution’s market capitalization (share price times the number of outstanding shares) to approximately $30 billion. That’s the midpoint of the $28 billion to $32 billion acquisition that Merck & Co. (NYSE: MRK) was pursuing for Revolution in January, according to the Financial Times. That prospective deal reportedly collapsed after the companies failed to agree on the value of daraxonrasib and Revolution’s other cancer-fighting candidates.

Merck never commented on its pursuit of Revolution, while AbbVie (NYSE: ABBV) flatly denied an earlier report that it sought to acquire the cancer drug developer. All the acquisition talk surrounding Revolution landed the company on GEN’s updated A-List Top 10 Takeover Targets of 2026, published March 9.

Cashing in

Revolution quickly cashed in on its positive data and stock surge, first proposing a $1 billion public offering of stock and debt, then doubling the size to $2 billion. The $2 billion offering consisted of concurrent public offerings of 10,563,381 shares of common stock at $142 per share (approximately $1.5 billion in gross proceeds) and $500 million of 0.50% convertible senior notes due 2033. Revolution also granted underwriters of the common stock offering a 30-day option to purchase up to an additional 1,584,506 shares.

J.P. Morgan, TD Cowen, and Guggenheim Securities are book-running managers for the stock and note offering, with LifeSci Capital acting as lead manager.

Daraxonrasib (formerly RMC-6236) is an oral RAS(ON) multi-selective, non-covalent inhibitor designed to target cancers driven by a variety of common RAS mutations, including PDAC, non-small cell lung cancer (NSCLC), and colorectal cancer. It is now under study in four global Phase III registrational trials—three in PDAC, the other in NSCLC. Daraxonrasib has been granted the FDA’s Breakthrough Therapy and Orphan Drug designations for the treatment of patients with previously treated metastatic PDAC harboring G12 mutations.

The RASolute 302 trial is a 501-patient global, randomized, registrational clinical study designed to evaluate the efficacy and safety of daraxonrasib as a monotherapy in patients with previously treated metastatic PDAC. Patients were randomized to receive either an oral dose of 300 mg daraxonrasib once daily or investigator’s choice of standard of care cytotoxic chemotherapy. The trial enrolled patients with metastatic PDAC harboring a wide range of RAS variants, including those with RAS G12 mutations (such as G12D, G12V, and G12R), as well as patients without an identified tumor RAS mutation (wild type).

Primary endpoints of RASolute 302 are OS and progression-free survival (PFS), as well as OS in patients with tumors harboring RAS G12 mutations. Secondary endpoints include PFS and OS in all enrolled patients (the intent-to-treat population) encompassing patients with and without identified tumor RAS mutations, as well as objective response rate, duration of response, and patient-reported quality of life.

Kailera makes history with $625M IPO

The “sign of life” StockWatch reported on last week when Avalyn Pharma filed paperwork for an initial public offering (IPO) is blooming this spring into a full blown comeback for IPOs, paced by what market watchers called the largest-ever public offering for a U.S. biotech—the eye-popping $625 million IPO carried out by Kailera Therapeutics—with at least two other companies submitting paperwork for filings of their own.

Kailera is a developer of therapies for obesity and weight management based on glucagon-like peptide receptor 1 (GLP-1) agonists, alone or in combination with glucose-dependent insulinotropic polypeptide (GIP) receptor agonists. The company priced an IPO on Thursday that generated $489.7 million in net proceeds through the sale of 39,062,500 shares of common stock at $16 per share—the high end of the pricing range of $14–$16.

On Kailera’s first full day of trading on Friday, investors showered the company with buys, propelling a 72% leap that sent shares to a high of $27.50 before the stock settled for a 62.5% gain, closing at an even $26.

The company earlier anticipated $458.7 million in net proceeds based on a $15 per share IPO price—though any $1 increase to the IPO price would increase what Kailera netted from the offering by an additional $31 million, according to an amended Form S-1 registration statement filed April 13 with the U.S. Securities and Exchange Commission (SEC).

Net proceeds could ultimately be even higher, since Kailera has granted its underwriters a 30-day option to purchase up to an additional 5,859,375 shares at the IPO price minus underwriting discounts and commissions. J.P. Morgan, Jefferies, Leerink Partners, TD Cowen, and Evercore ISI are joint book-running managers for the offering, with William Blair acting as lead manager.

Pipeline development

Kailera said the IPO plus its cash, cash equivalents, and marketable securities would give the company resources that it intended to spend on developing its four clinical-phase pipeline candidates, all in-licensed for $100 million upfront from Jiangsu Hengrui Pharmaceuticals (Shanghai Stock Exchange: 600276):

  • Ribupatide, the company’s lead product and a once-weekly injectable GLP-1/GIP receptor dual agonist peptide, including to fund three ongoing global Phase III KaiNETIC clinical trials into the second quarter of 2028 (more than $625 million, the estimate based on the $15 share price)
  • Oral ribupatide, a once-daily oral tablet formulation of ribupatide, including the funding of planned Phase III trials into the second quarter of 2028 (more than $150 million)
  • KAI-7535, a once-daily oral small molecule GLP-1 receptor agonist, including through the completion of a planned Phase II clinical trial (more than $50 million)
  • Other R&D activities, including development of KAI-4729, a once-weekly injectable GLP-1/GIP/glucagon receptor tri-agonist, as well as for working capital and other general corporate purposes (Remaining proceeds, not quantified)

Kailera gained exclusive global rights outside Greater China to Jiangsu Hengrui’s GLP-1 portfolio in 2024. That year, Kailera was launched with a $400 million Series A financing co-led by Atlas Venture, Bain Capital Life Sciences, and RTW Investments. Last October, Kailera garnered an additional $600 million in Series B financing led by a new investor, Bain Capital Private Equity.

“Our obesity-first approach seeks to capitalize on and improve upon proven science to advance product candidates which have the potential to maximize weight loss and address other critical needs in the current therapeutic landscape and to provide options, including oral options and alternative mechanisms, for people living with obesity no matter where they are in their treatment journey,” Kailera stated in its amended registration statement.

Kailera has adjusted the value of its cash and equivalents plus marketable securities from $652.728 million to a pro forma $1.142 billion in assets, reflecting the conversion of all outstanding preferred shares into common stock upon closing of the offering, plus an amended and restated certificate of incorporation.

Kailera’s IPO has surpassed the previous record-high among U.S. biotechs, the $604 million offering of Moderna (NASDAQ: MRNA) in December 2018, two years before the messenger RNA (mRNA) vaccine developer won FDA emergency authorization for its COVID-19 vaccine.

In the works

At least two other biotechs have filed Form S-1 registration statements for future IPOs in recent days, without disclosing how many shares they plan to raise or their offering prices.

  • Seaport Therapeutics is a developer of treatments for depression, anxiety, and other debilitating neuropsychiatric disorders based on its GlyphTM platform, a lymphatic-targeting prodrug technology designed to enhance a drug’s oral bioavailability and reduce side effects by bypassing first-pass metabolism. “Through our differentiated approach, we identify clinically validated mechanisms with established efficacy and safety profiles that have historically been limited by high first-pass metabolism, low bioavailability, and/or side effects,” Seaport stated in its Form S-1
  • Hemab Therapeutics, a developer of subcutaneous treatments for rare blood coagulation disorders, said its lead candidate, sutacimig (HMB-001), is a bispecific antibody in Phase I/II trials for the prophylactic treatment of Glanzmann thrombasthenia and Phase II studies for the prophylactic treatment of Factor VII deficiency. Another therapeutic candidate, HMB-002, is a monovalent antibody in Phase I/II trials for the subcutaneous prophylactic treatment of Von Willebrand disease. “We are building a franchise designed to address select coagulation disorders where we believe advances in biology, drug modality, and care delivery have the potential to meaningfully improve disease management,” Hemab stated in its Form S-1.

Leaders and laggards

  • MeiraGTx (NASDAQ: MGTX) shares yo-yoed, rising 26% from $8.97 to $11.29 Tuesday, after the company announced plans to present three-year data from its Phase I AQUAx trial (NCT04043104) evaluating AAV-hAQP1 in Grade 2/3 radiation-induced xerostomia. MeiraGTx reported “clinically meaningful” improvements in xerostomia symptoms, such as the average XQ score improving by 17 points (39.5%) at month 12, bilaterally treated participants reporting greater improvement than those treated unilaterally (21 points vs 13 points), and 75% of bilaterally-treated patients reporting transformative (≥10 point) improvement at month 12. After dipping 0.4% to $11.25 Wednesday, shares slumped 16% to $9.48 Thursday as MeiraGTx priced an approximately $100 million offering of 11,111,111 shares at $9 per share. Proceeds plus existing cash and cash equivalents are expected to fund commercial launches of AAV-hAQP1 and botaretigene sparoparvovec (“bota-vec”), a gene therapy for XLRP that MeiraGTx agreed to acquire from Johnson & Johnson (NYSE: JNJ) for $25 million cash upfront, a $50 million one-time payment tied to achieving specified regulatory and commercial milestones, plus a “mid-teens” royalty on global net sales starting on or after July 1, 2029.
  • Travere Therapeutics (NASDAQ: TVTX) shares soared 37% from $30.70 to $42.13 Tuesday after the rare disease drug developer won full FDA approval for Filspari® (sparsentan) in a second rare kidney disease. Filspari has become the first and only treatment for focal segmental glomerulosclerosis (FSGS), specifically to reduce proteinuria in adults and younger patients ages eight years and older with FSGS without nephrotic syndrome. Filspari won FSGS approval based on positive data from the Phase III DUPLEX trial (NCT03493685), where researchers reported a statistically significant 46% reduction in proteinuria from baseline to Week 108 in patients treated with Filspari vs. 30% for those treated with standard of care maximum labeled dose irbesartan, marketed by Sanofi (Euronext Paris: SAN) as Avapro®. Filspari first won FDA approval in 2023 to slow kidney function decline in adults with primary immunoglobulin A nephropathy (IgAN) who are at risk for disease progression.

The post StockWatch: Revolution’s Phase III Pancreatic Cancer Data Dazzles Investors, Analysts appeared first on GEN – Genetic Engineering and Biotechnology News.

The Download: bad news for inner Neanderthals, and AI warfare’s human illusion

This is today’s edition of The Download, our weekday newsletter that provides a daily dose of what’s going on in the world of technology.

The problem with thinking you’re part Neanderthal

There’s a theory that many of us have an “inner Neanderthal.” The idea is that Homo sapiens and a cousin species once bred, leaving some people today with a trace of Neanderthal DNA. 

This DNA is arguably the 21st century’s most celebrated discovery in human evolution. But in 2024, a pair of French geneticists called into question the theory’s very foundations. 

They proposed that what scientists interpret as interbreeding could instead be explained by population structure—the way genes concentrate in smaller, isolated groups.

Find out what it all means for human evolution.

—Ben Crair

This story is from the next issue of our print magazine, which is all about nature. Subscribe now to read it when it lands on Wednesday, April 22.

Why having “humans in the loop” in an AI war is an illusion

—Uri Maoz

AI is starting to shape real wars. It’s at the center of a legal battle between Anthropic and the Pentagon, playing a growing role in the conflict with Iran, and raising questions about how much humans should remain “in the loop.”

Under Pentagon guidelines, human oversight is meant to provide accountability, context, and security. But the idea of “humans in the loop” is a comforting distraction.

The real danger isn’t that machines will act without oversight; it’s that human overseers have no idea what the machines are actually “thinking.” Thankfully, science may offer a way forward.

Read the full op-ed on the urgent need for new safeguards around AI warfare.

The must-reads

I’ve combed the internet to find you today’s most fun/important/scary/fascinating stories about technology.

1 Despite blacklisting Anthropic, the White House wants its new model
Trump officials are negotiating access to Mythos. (Axios)
+ Anthropic said it was too dangerous for a public release. (Bloomberg $)
+ Finance ministers are alarmed about the security risks. (BBC)
+ Anthropic just rolled out a model that’s less risky than Mythos. (CNBC)
+ The Pentagon has pursued a culture war against the company. (MIT Technology Review)

2 Sam Altman’s side hustles have raised conflict-of-interest concerns
His opaque investments could influence decisions at OpenAI. (WSJ $)
+ A jury will soon decide if OpenAI abandoned its founding mission. (Wired $)
+ The company is making a big play for science. (MIT Technology Review)

3 A Starlink outage during drone tests exposed the Pentagon’s SpaceX reliance
It was one of several Navy test disruptions linked to Starlink. (Reuters $)
+ The DoD is also tapping Ford and GM for military innovations.(NYT $)

4 Data center delays threaten to choke AI expansion
40% of this year’s projects are at risk of falling behind schedule. (FT $)
+ Partly because no one wants a data center in their backyard. (MIT Technology Review)

5 Alibaba just released its own version of a world model
Happy Oyster is the latest attempt to extend AI’s ability to comprehend physical reality. (SCMP)
+ But they still need to understand cause and effect. (FT $)

6 Google’s Gemini is now generating AI images tailored to personal data
By analyzing users’ Google services and data. (Quartz)
+ Google says it will cut the need for detailed prompts. (TechCrunch)

7 OpenAI is beefing up its agentic coding and development system
Its Codex update is a direct shot at Claude Code. (The Verge)
+ But not everyone is convinced about AI coding. (MIT Technology Review)

8 Europe’s online age verification app is here
It’s available for free to any company that wants it. (Wired $) 

9 Smartglasses are giving Korean theaters hope of a K-Pop moment
Their AI-powered translations are taking the shows to the world. (NYT $)

10 Global voice actors are fighting Hollywood’s AI push
Their voices are training the models that are replacing them. (Rest of World)

Quote of the day

“There’s this dark period between now and some time in the future where the advantage is very much offensive AI.” 

—Rob Joyce, former director of cybersecurity at the National Security Agency, tells Bloomberg how AI is creating new hacking threats.

One More Thing

COURTESY OF NOVEON MAGNETICS


The race to produce rare earth elements

Access to rare earth elements will determine which countries meet their goals for lowering emissions or generating energy from non-fossil-fuel sources. But some nations, including the US, are worried about the supply of these elements. 

China dominates the market, while extraction in the US is limited. As a result, scientists and companies are exploring unconventional sources. Read the full story on their search for critical minerals.


—Mureji Fatunde

We can still have nice things

A place for comfort, fun and distraction to brighten up your day. (Got any ideas? Drop me a line.)

+ This ska cover of Rage Against the Machine is an upbeat way to start a revolution.
+ We finally know how far Stretch Armstrong can really stretch.
+ Customize these ambient sounds to wash away disruptive thoughts.
+ Here’s proof childhood dreams can come true: a girl guiding a seal to perform tricks. 

Cancer Cell Apoptosis Avoided by Membrane Oligomerization

Apoptosis in cancer cells may be easier to unleash than previously thought, according to new research led by scientists at Umeå University and collaborators. That finding could open up more cancers to treatment with anti-apoptotic drugs. The team used neutron reflectometry (NR) and ATR-FTIR to detail communication between proteins in and around the mitochondrial outer membrane (MOM). 

“We use neutrons as a kind of ‘x-ray’ magnifying glass to study how various proteins talk to each other inside the cell,” Gerhard Gröbner, PhD, told Inside Precision Medicine. He is a professor at Umeå University and senior author of a new study that looks at the role of the Bax protein in apoptosis. The findings appear in ACS Chemical Biology.

Apoptosis is a form of programmed cell death that removes old or damaged cells, enabling the immune system to function properly. When apoptosis does not work as it should, as in many cancers, cells can divide uncontrollably and form tumors.

Many cancer therapies (e.g. drugs and radiation) are designed to trigger apoptosis in tumors. But there are also many aggressive and often incurable cancers that current anti-apoptotic therapies do not work on due to these tumors’ intensive use of survival proteins, such as Bcl-2 and its relatives, which can stop apoptotic death.

“Finding new drugs to inhibit Bcl-2 and its relatives in a wider sense would thus help treat more cancers. Currently only one Bcl-2 drug is available, and it is used for very specific leukemia,” said Gröbner.

“Going forward we will test a range of potential drug candidates to block Bcl-2 to release cell-killing proteins like Bax again to improve therapies,” he added.

The cell‑killing protein Bax protein is one of the most important proteins controlling apoptosis. Once activated, Bax can initiate apoptosis by forming pores in the membranes of mitochondria. Another key protein from the same family, the cell‑protective protein Bcl‑2, instead prevents Bax from killing tumor cells. In nearly half of all human cancers, one of the underlying problems is an increased production of Bcl‑2, which promotes tumor growth and often leads to poor response to therapy.

“In our research, we have used advanced neutron experiments to show how Bcl‑2 protects cancer cells by blocking the death‑inducing proteins that are most often activated by therapy,” said Gröbner.

The team used NR and ATR-FTIR to elucidate the molecular communication between those proteins in and around the mitochondrial outer membrane (MOM). The spatial and temporal changes across model MOM surfaces were resolved during the interaction of Bax with Bcl-2. The NR-derived membrane surface Bax distributions suggested that Bcl-2 mediated Bax sequestration through both Bcl-2/Bax heterodimerization and Bax/Bax oligomerization. Kinetic analysis revealed a two-step process: rapid formation of Bcl-2/Bax heterodimers, followed by slower Bax oligomerization on these complexes

The experiments show that Bcl‑2 can capture and bind several Bax proteins at the same time. This makes the inhibition of cell death more efficient than previously thought. Cancer cells do not need to produce extremely large amounts of Bcl‑2 to protect themselves—even a moderate increase can be sufficient.

The researchers also investigated how the composition of the mitochondrial membrane affects the interaction between the proteins. They found one particular lipid, cardiolipin, can promote apoptosis and help Bax form pores in the membrane. However, even in membranes containing cardiolipin, a sufficiently high level of Bcl‑2 can still prevent cell death.

“In the longer term, this type of knowledge could open up new opportunities for cancer treatment, for example by targeting Bcl‑2 and its protective function,” says Gröbner.

The study was carried out in collaboration between researchers from Umeå University, Lund University, the European Spallation Source (ESS) in Lund, the ISIS Neutron and Muon Source and Diamond Light Source in the United Kingdom, and the Institut Laue‑Langevin (ILL) in France.

 

The post Cancer Cell Apoptosis Avoided by Membrane Oligomerization appeared first on Inside Precision Medicine.

No one’s sure if synthetic mirror life will kill us all

For four days in February 2019, some 30 synthetic biologists and ethicists hunkered down at a conference center in Northern Virginia to brainstorm high-risk, cutting-­edge, irresistibly exciting ideas that the National Science Foundation should fund. By the end of the meeting, they’d landed on a compelling contender: making “mirror” bacteria. Should they come to be, the lab-created microbes would be structured and organized like ordinary bacteria, with one important exception: Key biological molecules like proteins, sugars, and lipids would be the mirror images of those found in nature. DNA, RNA, and many other components of living cells are chiral, which means they have a built-in rotational structure. Their mirrors would twist in the opposite direction. 

Researchers thrilled at the prospect. “Everybody—everybody—thought this was cool,” says John Glass, a synthetic biologist at the J. Craig Venter Institute in La Jolla, California, who attended the 2019 workshop and is a pioneer in developing synthetic cells. It was “an incredibly difficult project that would tell us potentially new things about how to design and build cells, or about the origin of life on Earth.” The group saw enormous potential for medicine, too. Mirror microbes might be engineered as biological factories, producing mirror molecules that could form the basis for new kinds of drugs. In theory, such therapeutics could perform the same functions as their natural counterparts, but without triggering unwelcome immune responses. 

After the meeting, the biologists recommended NSF funding for a handful of research groups to develop tools and carry out preliminary experiments, the beginnings of a path through the looking glass. The excitement was global. The National Natural Science Foundation of China funded major projects in mirror biology, as did the German Federal Ministry of Research, Technology, and Space.

By five years later, in 2024, many researchers involved in that NSF meeting had reversed course. They’d become convinced that in the worst of all possible futures, mirror organisms could trigger a catastrophic event threatening every form of life on Earth; they’d proliferate without predators and evade the immune defenses of people, plants, and animals. 

“I wish that one sunny afternoon we were having coffee and we realized the world’s about to end, but that’s not what happened.”

Kate Adamala, synthetic biologist, University of Minnesota

Over the past two years, they’ve been ringing alarm bells. They published an article in Science in December 2024, accompanied by a 299-page technical report addressing feasibility and risks. They’ve written essays and convened panels and cofounded the Mirror Biology Dialogues Fund (MBDF), a broadly funded nonprofit charged with supporting work on understanding and addressing the risk. The issue has received a blaze of media attention and ignited dialogues among not only chemists and synthetic biologists but also bioethicists and policymakers.  

What’s received less attention, however, is how we got here and what uncertainties still remain about any potential threat. Creating a mirror-life organism would be tremendously complicated and expensive. And although the scientific community is taking the alarm seriously, some scientists doubt whether it’s even possible to create a mirror organism anytime soon. “The hypothetical creation of mirror-­image organisms lies far beyond the reach of present-day science,” says Ting Zhu, a molecular biologist at Westlake University, in China, whose lab focuses on synthesizing mirror-image peptides and other molecules. He and others have urged colleagues not to let speculation and anxiety guide decision-making and argued that it’s premature to call for a broad moratorium on early-stage research, which they say could have medical benefits. 

But the researchers who are raising flags describe a pathway, even multiple pathways, to bringing mirror life into existence—and they say we urgently need guardrails to figure out what kinds of mirror-biology research might still be safe. That means they’re facing a question that others have encountered before, multiple times over the last several decades and with mixed results—one that doesn’t have a neat home in the scientific method. What should scientists do when they see the shadow of the end of the world in their own research? 

Looking-glass life

The French chemist and microbiologist Louis Pasteur was the first to recognize that biological molecules had built-in handedness. In the late 19th century, he described all living species as “functions of cosmic asymmetry.” What would happen, he mused, if one could replace these chiral components with their mirror opposites? 

Scientists now recognize that chirality is central to life itself, though no one knows why. In humans, 19 of the 20 so-called “standard” amino acids that make up proteins are chiral, and all in the same way. (The outlier, glycine, is symmetrical.) The functions of proteins are intricately tied to their shapes, and they mostly interact with other molecules through chiral structures. Almost all receptors on the surface of a cell are chiral. During an infection, the immune system’s sentinels use chirality to detect and bind to antigens—substances that trigger an immune response—and to start the process of building antibodies. 

By the late 20th century, researchers had begun to explore the idea of reversing chirality. In 1992, one team reported having synthesized the first mirror-image protein. That, in turn, set off the first clarion call about the risk: In response to the discovery, chemists at Purdue University pointed out, briefly, that mirror-life organisms, if they escaped from a lab, would be immune to any attack by “normal” life. A 2010 story in Wired highlighting early findings in the area noted that if a such a microbe developed the ability to photosynthesize, it could obliterate life as we know it. 

The synthetic biology community didn’t seriously weigh those threats then, says David Relman, a specialist who bridges infectious disease and microbiology at Stanford University and a trailblazer in studying the gut and oral microbiomes. The idea of a mirror microbe seemed too far beyond the actual progress on proteins. “This was almost a solely theoretical argument 20 years ago,” he says. 

Now the research landscape has changed. 

Scientists are quickly making progress on mirror images of the machinery cells use to make proteins and to self-replicate. Those components include DNA, which encodes the recipes for proteins; DNA polymerases, which help copy genetic material; and RNA, which carries recipes to ribosomes, the cell’s protein factories. If researchers could make self-replicating mirror ribosomes, then they would have an efficient way to produce mirror proteins. That could be used as a biological manufacturing method for therapeutics. But embedded in a self-­replicating, metabolizing synthetic cell, all these pieces could give rise to a mirror microbe. 

When synthetic biologists convened in Northern Virginia in 2019, they didn’t recognize how quickly the technology was advancing, and if they saw a threat at all, it may have been obscured by the blinding appeal of pushing the science forward. What’s become apparent now, says Glass, is that scientists in different disciplines, all related to mirror life, were largely unaware of what other scientists had been doing. Chemists didn’t know that synthetic biologists had made so much progress on creating mirror cells with natural chirality from scratch. Biologists didn’t appreciate that chemists were building ever-larger mirror macromolecules. “We tend to be siloed,” Glass says. And nobody, he says, had thought to seriously examine the immune system concerns that had already been raised in response to earlier work. “There was not an immunologist or an infectious disease person in the room,” Glass says, reflecting on the 2019 meeting. “I may have come closest, given that I work with pathogenic bacteria and viruses,” he adds, but his work doesn’t address how they cause infections in their hosts.

on the left, a hand with petri dish and the same image inverted on the right

GETTY IMAGES

These scientists also didn’t know that around the same time as their meeting, another conversation about mirror life was happening—a darker dialogue that was as focused on danger as it was on discovery. Starting around 2016, researchers with a nonprofit called Open Philanthropy had begun compiling research files on catastrophic biological risks. The organization, which rebranded as Coefficient Giving in 2025, funds projects across a range of focus areas; it adheres to a divisive philanthropic philosophy called effective altruism, which advocates giving money to projects with the highest potential benefit to the most people. While that might not sound objectionable, critics point out that the metrics devotees use to gauge “effectiveness” can prioritize long-term solutions while neglecting social injustices or systemic problems. 

Someone in Open Philanthropy’s bio­security group had suggested looking into the risks posed by mirror life. In 2019 the organization began funding research by Kevin Esvelt, who leads the Sculpting Evolution group at the MIT Media Lab, on biosecurity issues, including mirror life. He began reading up to see whether mirror life was something to worry about.

Esvelt made waves in 2013 for pioneering the use of CRISPR to develop a gene drive, a technology that could spread genetic changes introduced into a living organism through a whole population. Researchers are exploring its use, for example, to make mosquitoes hostile to the parasite that causes malaria—and, as a result, lower their chance of spreading it to humans. But almost immediately after he developed the tool, Esvelt argued against using it for profit, at least until proper safeguards could be set and its use in fighting malaria had been established. “Do you really have the right to run an experiment where if you screw up, it affects the whole world?” he asked, in this magazine, in 2016. At the Media Lab, Esvelt leads efforts to safely develop gene drives that can be deployed locally but prevented from spreading globally. 

Esvelt says he’s often thinking about the security risks posed by self-sustaining genetically engineered technologies, and research led him to suspect that the threat of mirror organisms hadn’t been seriously interrogated. The more he learned about microbial growth rates, predator-prey and microbe-microbe interactions, and immunology, the more he began to worry that mirror organisms, if impervious to the innate defenses of natural ones, could cause unstoppable infections in the event that they escaped the lab. 

Even if the first experimental iteration of such a germ were too fragile to survive in the environment or a human body, Esvelt says, it would be a light lift to genetically engineer new, more resilient versions with existing technology. Even worse, he says, the results could be weaponized. The possible path from 2019 to global annihilation seemed almost too direct, he found. 

But he wasn’t an expert in all the scientific fields involved in research on mirror life, so he started making calls. He first described his concerns to Relman one night in February 2022, at a restaurant outside Washington, DC. Esvelt hoped Relman would tell him he was wrong, that he’d missed something over the years of gathering data. Instead, he was troubled. 

The concern spreads

When Relman returned to California, he read more about the technology, the risks, and the role of chirality in the immune system and the environment. And he consulted experts he knew well—ecologists, other microbiologists, immunologists, all of them leaders in their fields—in an attempt to assuage his concerns. “I was hoping that they’d be able to say, I’ve thought about this, and I see a problem with your logic. I see that it’s really not so bad,” he says. “At every turn, that did not happen. Something about it was new to every person.” 

The concern spread. Relman worked with Jack Szostak, a professor of chemistry at the University of Chicago, and a group of researchers to see if it was possible to make an argument that mirror life wasn’t going to wipe out humanity. Included in that group was Kate Adamala, a synthetic biologist at the University of Minnesota. She was a natural choice: Adamala had shared the initial grant from the NSF, in 2019, to explore mirror-life technologies. 

She also became convinced the risk was real—and was dumbfounded that she hadn’t seen it earlier. “I wish that one sunny afternoon we were having coffee and we realized the world’s about to end, but that’s not what happened,” she says. “I’m embarrassed to admit that I wasn’t even the one that brought up the risks first.” Through late 2023 and early 2024, the endeavor began to take on the form of a rigorous scientific investigation. Experts were presented with a hypothesis—namely, that if mirror cells were built, they would pose an existential threat—and asked to challenge it. The goal was to falsify the hypothesis. “It would be great if we were wrong,” says Vaughn Cooper, a microbiologist at the University of Pittsburgh and president-elect of the American Society for Microbiology. 

Relman says that as the chemists and biologists learned more about one another’s work and began to understand what immunologists know about how living things defend themselves, they started to connect the dots and see an emerging picture of an unstoppable synthetic threat.

Some scientists have pushed back against the doomsday scenario, suggesting that the case against mirror life offers an “inflated view of the danger.”

Timothy Hand, an immunologist at the University of Pittsburgh who hadn’t participated in the 2019 NSF meeting, wasn’t initially worried when he heard about mirror life, in 2024. “The mammalian immune system has this incredible capability to make antibodies against any shape,” he says. “Who cares if it’s a mirror?” But when he took a closer look at that process, he could see a cascade of potential problems far upstream of antibody production. Start with detection: Macrophages, which are cells the immune system uses to identify and dispatch invaders, use chiral sensing receptors on their surfaces. The proteins they use to grab on to those invaders, too, are chiral. That suggests the possibility that an organism could be infected with a mirror organism but not be able to detect it or defend against it. “The lack of innate immune sensing is an incredibly dangerous circumstance for the host,” Hand says.

By early 2024, Glass had become concerned as well. Relman and James Wagstaff, a structural biologist from Open Philanthropy, visited him at the Venter Institute to talk about the possibility of using synthetic cell technology—Glass’s specialty—to build mirror life. “At first I thought, This can’t be real,” Glass says. They walked through arguments and counterarguments. “The more this went on, the more I started feeling ill,” he says. “It made me realize that work I had been doing for much of the last 20 years could be setting the world up for this incredible catastrophe.” 

In the second half of 2024, the growing group of scientists assembled the report and wrote the policy forum for Science. Relman briefed policymakers at the White House, members of the defense community, and the National Security Agency. Researchers met with the National Institutes of Health and the National Science Foundation. “We briefed the United Nations, the UK government, the government of Singapore, scientific funding organizations from Brazil,” says Glass. “We’ve talked to the Chinese government indirectly. We were trying to not blindside anybody.” 

A year and a half on, the push has had an impact. UNESCO has recommended a precautionary global moratorium on creating mirror-life cells, and major philanthropic organizations that fund science, including the Alfred P. Sloan Foundation, have announced they will not finance research leading to a mirror microorganism. The Bulletin of the Atomic Scientists highlighted considerations about mirror life in its most recent report on the Doomsday Clock. In March, the United Nations Secretary-General’s Scientific Advisory Board issued a brief highlighting the risks—noting, for example, that recent progress on building mirror molecules could reduce the cost of creating a mirror microbe. 

“I think no one really believes at this stage that we should make mirror life, based on the evidence that’s available,” says James Smith, the scientist who leads the MBDF, the nonprofit focused on assessing the risks of mirror life, which is funded by Coefficient Giving, the Sloan Foundation, and other organizations. The challenge now, Smith says, is for scientists to work with policymakers and bioethicists to figure out how much research on mirror life should be permitted—and who will enforce the rules.

Drawing the line

Not everyone is convinced that mirror organisms pose an existential threat. It’s difficult to verify predictions about how mirror microbes would fare in the immune system—or the larger world—without running experiments on them. Some scientists have pushed back against the doomsday scenario, suggesting that the case against mirror life offers an “inflated view of the danger.” Others have noted that carbohydrates called glycans already exist in both left- and right-handed forms—even in pathogens—and the immune system can recognize both of them. Experiments focused on interactions between the immune system and mirror molecules, they say, could help clarify the risks of mirror organisms and reduce uncertainty. 

Even among those convinced that the worst-case scenario is possible, researchers still disagree over where to draw the line. What inquiries should be allowed and what should be prohibited?

Andy Ellington, a biotechnologist and synthetic biologist at the University of Texas at Austin, doesn’t think mirror organisms will come to fruition anytime soon. Even if they do, he isn’t sure they will pose a threat. “If there is going to be harm done to the human race, this is about position 382 on my list,” he says. But at the same time, he says it’s a complicated issue worth studying more, and he wants to see the conversations continue: “We’re operating in a space where there’s so much unknown that it’s very difficult for us to do risk assessment.” 

Even among those convinced that the worst-case scenario is possible, researchers still disagree over where to draw the line. What inquiries should be allowed and what should be prohibited? 

Adamala, of the University of Minnesota, and others see a natural line at ribosomes, the cellular factories that transform chains of amino acids into proteins. These would be a critical ingredient in creating a self-replicating organism, and Adamala says the path to getting there once mirror ribosomes are in place would be pretty straightforward. But Zhu, at Westlake, and others counter that it’s worth developing mirror ribosomes because they could possibly produce medically useful peptides and proteins more efficiently than traditional chemical methods. He sees a clear distinction, and a foundational gap, between that kind of technology and the creation of a living synthetic organism. “It is crucial to distinguish mirror-image molecular biology from mirror-image life,” he says. That said, he points out that many synthetic molecules and organisms containing unnatural components, including but not limited to the mirror-image subset, might pose health risks. Researchers, he says, should focus on developing holistic guidelines to cover such risks—not just those from mirror molecules. 

Even if the exact risk remains uncertain, Esvelt remains more convinced than ever that the work should be paused, perhaps indefinitely. No one has taken a meaningful swing at the hypothesis that mirror life could wipe out everything, he says. The primary uncertainties aren’t around whether mirror life is dangerous, he points out; they have more to do with identifying which bacterium—including what genes it encodes, what it eats, how it evades the immune system’s sentinels—could lead to the most serious consequences. “The risk of losing everything, like the entire future of humanity integrated over time, is not worth any small fraction of the economy. You just don’t muck around with existential risk like that,” he says. 

In some ways, scientists have been here before, working out rules and limits for research. Two years after the start of the covid-19 pandemic, for example, the World Health Organization published guidelines for managing risks in biological research. But the history is much deeper: Horrific episodes of human experimentation led to the establishment of institutional review boards to provide ethical oversight. In the early 1970s, in response to concerns over lab-acquired infections and growing use of biological warfare, the US Centers for Disease Control and Prevention established biohazard safety levels (BSLs), which govern work on potentially dangerous biological experiments.

And in 1975—at the dawn of recombinant DNA research, which allows researchers to put genetic material from one organism into another—geneticists met at the Asilomar conference center in Pacific Grove, California, to hammer out rules governing the work. There were concerns over what would happen if some virus or bacterium, genetically engineered to have traits that would make it particularly dangerous for people, escaped from a lab. Scientists agreed to self-imposed restrictions, like a moratorium on research until new safety guidelines were in place. As a result of the meeting, in June 1976 the NIH issued rules that, among other things, categorized the risks associated with rDNA experiments and aligned them with the newly adopted BSL system.

Asilomar is often hailed as a successful model for scientific self-governance. But that perception reflects a tendency to recall the meeting through a nostalgic haze. “In fact, it was incredibly messy and human,” says Luis Campos, a historian of science at Rice University. Equally brilliant Nobelists argued on either side of the question of whether to rein in rDNA research. Technical discussions dominated; talks about who would be affected by the technology were missing. The meeting didn’t start establishing guidelines, says Campos, until the lawyers mentioned liability and lab leaks. 

For now it’s unclear whether these examples of self-­governance, which arose from the demonstrated risks of existing technologies, hold useful lessons for the mirror-life community. Three competing images of the future are coming into focus: Mirror life might not be possible, it might be possible but not threatening, or it might be possible and capable of obliterating all life on Earth. 

Scientists may be censoring themselves out of fear and speculation. To some, shutting down the work seems necessary and urgent; to others, it is unnecessarily limiting. What’s clear is that the question of what to do about mirror life has been both illuminating and disorienting, pushing scientists to interrogate not only their current research but where it might lead. This is uncharted territory. 

Stephen Ornes is a science writer based in Nashville, Tennessee.

The problem with thinking you’re part Neanderthal

You’ve probably heard some version of this idea before: that many of us have an “inner Neanderthal.” That is to say, around 45,000 years ago, when Homo sapiens first arrived in Europe, they met members of a cousin species—the broad-browed, heavier-set Neanderthals—and, well, one thing led to another, which is why some people now carry a small amount of Neanderthal DNA. 

This DNA is arguably the 21st century’s most celebrated discovery in human evolution. It has been connected to all kinds of traits and health conditions, and it helped win the Swedish geneticist Svante Pääbo a Nobel Prize.

But in 2024, a pair of French population geneticists called into question the foundation of the popular and pervasive theory. 

Lounès Chikhi and Rémi Tournebize, then colleagues at the Université de Toulouse, proposed an alternative explanation for the very same genomic patterns. The problem, they said, was that the original evidence for the inner Neanderthal was based on a statistical assumption: that humans, Neanderthals, and their ancestors all mated randomly in huge, continent-size populations. That meant a person in South Africa was just as likely to reproduce with a person in West Africa or East Africa as with someone from their own community. 

Archaeological, genetic, and fossil evidence all shows, though, that Homo ­sapiens evolved in Africa in smaller groups, cut off from one another by deserts, mountains, and cultural divides. People sometimes crossed those barriers, but more often they partnered up within them. 

In the terminology of the field, this dynamic is called population structure. Because of structure, genes do not spread evenly through a population but can concentrate in some places and be totally absent from others. The human gene pool is not so much an Olympic-size swimming pool as a complex network of tidal pools whose connectivity ebbs and flows over time.

This dynamic greatly complicates the math at the heart of evolutionary biology, which long relied on assumptions like randomly mating populations to extract general principles from limited data. If you take structure into account, Chikhi told me recently, then there are other ways to explain the DNA that some living people share with Neanderthals—ways that don’t require any interspecies sex at all.

“I believe most species are spatially organized and structured in different, complex ways,” says Chikhi, who has researched population structure for more than two decades and has also studied lemurs, orangutans, and island birds. “It’s a general failure of our field that we do not compare our results in a clear way with alternative scenarios.” (Pääbo did not respond to multiple requests for comment.)

The inner Neanderthal became a story we could tell ourselves about our flaws and genetic destiny: Don’t blame me; blame the prognathic caveman hiding in my cells.

Chikhi and Tournebize’s argument is about population structure, yes, but at heart, it is actually one about methods—how modern evolutionary science deploys computer models and statistical techniques to make sense of mountains upon mountains of genetic data. 

They’re not the only scientists who are worried. “People think we really understand how genomes evolve and can write sophisticated algorithms for saying what happened,” says William Amos, a University of Cambridge population geneticist who has been critical of the “inner Neanderthal” theory. But, he adds, those models are “based on simple assumptions that are often wrong.” 

And if they’re wrong, what’s at stake is far more than a single evolutionary mystery. 

A captivating story of interspecies passion

Back in 2010, Pääbo’s lab pulled off something of a miracle. The researchers were able to extract DNA from nuclei in the cells of 40,000-year-old Neanderthal bones. DNA breaks down quickly after death, but the group got enough of it from three different individuals to produce a draft sequence of the entire Neanderthal genome, with 4 billion base pairs. 

As part of their study, they performed a statistical test comparing their Neanderthal genome with the genomes of five present-day people from different parts of the world. That’s how they discovered that modern humans of non-African ancestry had a small amount of DNA in common with Neanderthals, a species that diverged from the Homo sapiens line more than 400,000 years ago, that they did not share with either modern humans of African ancestry or our closest living relative, the chimpanzee. 

Neanderthal front and profile view
This model of a Neanderthal man was exhibited in the “Prehistory Gallery” at London’s Wellcome Historical Medical Museum in the 1930s.
WELLCOME COLLECTION

Pääbo’s team interpreted this as evidence of sexual reproduction between ancient Homo sapiens and the Neanderthals they encountered after they expanded out of Africa. “Neanderthals are not totally extinct,” Pääbo said to the BBC in 2010. “In some of us, they live on a little bit.”

The discovery was monumental on its own—but even more so because it reversed a previous consensus. More than a decade earlier, in 1997, Pääbo had sequenced a much smaller amount of Neanderthal DNA, in that case from a cell structure called a mitochondrion. It was different enough from Homo sapiens mitochondrial DNA for his team to cautiously conclude there had been “little or no interbreeding” between the two species. 

After 2010, though, the idea of hybridization, also called admixture, effectively became canon. Top journals like Science and Nature published study after study on the inner Neanderthal. Some scientists have argued that Homo sapiens would never have adapted to colder habitats in Europe and Asia without an infusion of Neanderthal DNA. Other research teams used Pääbo’s techniques to find genetic traces of interbreeding with an extinct group of hominins in Asia, called the Denisovans, and a mysterious “ghost lineage” in Africa. Biologists used similar tests to find evidence of interbreeding between chimpanzees and bonobos, polar and brown bears, and all kinds of other animals. 

The inner-Neanderthal hypothesis also took a turn for the personal. Various studies linked Neanderthal DNA to a head-spinning range of conditions: alcoholism, asthma, autism, ADHD, depression, diabetes, heart disease, skin cancer, and severe covid-19. Some researchers suggested that Neanderthal DNA had an impact on hair and skin color, while others assigned individuals a “NeanderScore” that was correlated with skull shape and prevalence of schizophrenia markers. Commercial genetic testing companies like 23andMe started offering customers Neanderthal ancestry reports. 

The inner Neanderthal became a story we could tell ourselves about our flaws and genetic destiny: Don’t blame me; blame the prognathic caveman hiding in my cells. Or as Latif Nasser, a host of the popular-science program Radiolab, put it when he was hospitalized with Crohn’s disease, another Neanderthal-associated condition: “I just keep imagining these tiny Neanderthals … just, like, stabbing me and drawing these little droplets of blood out of me.”

“These things become meaningful to people,” Chikhi says. “What we say will be important to how people view themselves.” 

The pitfalls of simplistic solutions 

When population geneticists built the theoretical framework for evolutionary biology in the early 20th century, genes were only abstract units of heredity inferred from experiments with peas and fruit flies. Population genetics developed theory far more quickly than it accumulated data. As a result, many data-driven scientists dismissed the study of evolution as a form of storytelling based on unexamined assumptions and preconceived ideas.

By the ’90s, though, genes were no longer abstractions but sequenced segments of DNA. Genomic sequencing grounded evolutionary studies in the kind of hard data that a chemist or physicist could respect. 

Yet biologists could not simply read evolutionary history from genomes as though they were books. They were trying to determine which of a nearly infinite number of plausible histories was the most likely to have created the patterns they observed in a small sample of genomes. For that, they needed simplified, algorithmic models of evolution. The study of evolution shifted from storytelling to statistics, and from biology to computer science. 

That suited Chikhi, who as a child was drawn to the predictable laws and numerical precision of math and science. He entered the field in the mid-’90s just as the first big studies of human DNA were settling old debates about human origins. DNA showed that Africa harbored far more genetic diversity than the entire rest of the planet. The new evidence supported the idea that modern humans evolved for hundreds of thousands of years in Africa and expanded to the other continents only in the last 100,000 years. For Chikhi, whose parents were Algerian immigrants, this discovery was a powerful challenge to the way some archaeologists and biologists talked about race. DNA could be used to deconstruct rather than encourage the pernicious idea that human races had deep-seated evolutionary differences based on their places of origin. 

At the same time, though, he was wary of the tendency to treat DNA as the final verdict on open questions in evolution. Chikhi had been surprised when, back in 1997, Pääbo and his team used that small amount of mitochondrial DNA to rule out hybridization between Homo sapiens and Neanderthals. He didn’t think that the absence of Neanderthal DNA there necessarily meant it wouldn’t be found elsewhere in the Homo sapiens genome.

Chikhi’s own research in the aughts opened his eyes to the gaps between historical reality and models of evolution. For one, despite the assumption of random mating, none of the animals Chikhi studied actually mated randomly. Orangutans lived in highly fragmented habitats, which restricted their pool of potential mates, and female birds were often extremely picky about their male partners. 

These factors could confound an evolutionary biologist’s traditional statistical tool kit. Scientists were starting to apply a mathematical technique to estimate historical population sizes for a species from the genome of just a single individual. This method showed sharp population declines in the histories of many different species. Chikhi realized, though, that the apparent declines could be an artifact of treating a structured population as one that evolved with random mating; in that case, the technique could indicate a bottleneck even if all the subgroups were actually growing in size. “This is completely counterintuitive,” he says. 

That’s at least partly why, when Pääbo’s 2010 Neanderthal genome came out, Chikhi was impressed with the sheer technical accomplishment but also leery of the findings about hybridization. “It was the type of thing we conclude too quickly based on genetic data,” he says. Pääbo’s work mentioned population structure as a possible alternative explanation—but didn’t follow up.

Just a couple of years later, a pair of independent scientists named Anders Eriksson and Andrea Manica picked up the idea, building a model with simple population structure that explicitly excluded admixture. They simulated human evolution starting from 500,000 years ago and found that their model produced the same genomic patterns Pääbo’s group had interpreted as evidence of hybridization.

“Working with structured models is really out of the comfort zone of a lot of population geneticists,” says Eriksson, now a professor at the University of Tartu in Estonia.

Their research impressed Chikhi. “At the time, I thought people would focus on population structure in the evolution of humans,” he says. Instead, he watched as the inner-Neanderthal hypothesis took on a life of its own. Scientists produced new methods to quantify hybridization but rarely examined whether population structure would yield the same results. To Chikhi, this wasn’t science; it was storytelling, like some of the old narratives about the evolution of racial differences. 

Chikhi and Tournebize decided to take a crack at the problem themselves. “I’ve always been very skeptical about science, and population genetics in particular,” says Tournebize, now a researcher at the French National Research Institute for Sustainable Development. “We make a lot of assumptions, and the models we use are very simplistic.” As detailed in a 2024 paper published in Nature Ecology & Evolution, they built a model of human evolution that replaced randomly mating continent-wide populations with many smaller populations linked by occasional migration. Then they let it run—a million times.

At the end of the simulation, they kept the 20 scenarios that produced genomes most similar to the ones in a sample of actual Homo sapiens and Neanderthals. Many of these scenarios produced long segments of DNA like the ones their peers argued could only have been inherited from Neanderthals. They showed that several statistics, which other scientists had proposed as measurements of Neanderthal DNA, couldn’t actually distinguish between hybridization and population structure. What’s more, they showed that many of the models that supported hybridization failed to accurately predict other known features of human evolution.

“A model will say there was admixture but then predict diversity that is totally incompatible with what we actually know of human diversity,” Chikhi says. “Nobody seems to care.”

So how did Neanderthal DNA wind up in living people if not via interspecies passion? Chikhi and Tournebize think it’s more likely that it was inherited by both Neanderthals and some sapiens groups in Africa from a common ancestor living at least half a million years ago. If the sapiens groups carrying those genetic variants included the people who migrated out of Africa, then the two human species would have already had the DNA in common when they came into contact in Europe and Asia—no sex required. 

“The interpretation of genetic data is not straightforward,” Chikhi says. “We always have to make assumptions. Nobody takes data and magically comes up with a solution.” 

Embracing the uncertainty 

Most of the half-dozen population geneticists I spoke with praised Chikhi and Tournebize’s ingenuity and appreciated the spirit of their critique. “Their paper forces us to think more critically about the model we use for inference and consider alternatives,” says Aaron Ragsdale, a population geneticist at the University of Wisconsin–Madison. His own work likewise suggests that the earliest Homo sapiens populations in Africa were probably structured—and that this is the likely reason for genomic patterns that other research groups had attributed to hybridization with a mysterious “ghost lineage” of hominins in Africa.

Yet most researchers still believe that modern humans and Neanderthals did probably have children with each other tens of thousands of years ago. Several pointed to the fact that fossil DNA of Homo sapiens who died thousands of years ago had longer chunks of apparent Neanderthal DNA than living people, which is exactly what you would expect if they had a more recent Neanderthal ancestor. (To address this possibility, Chikhi and Tournebize included DNA from 10 ancient humans in their study and found that most of them fit the structured model.) And while the Harvard population geneticist David Reich, who helped design the statistical test from Pääbo’s 2010 study, declined an interview, he did say he thought Chikhi and Tournebize’s model was “weak” and “very contrived,” adding that “there are multiple lines of evidence for Neanderthal admixture into modern humans that make the evidence for this overwhelming.” (Two other authors of that study, Richard Green and Nick Patterson, did not respond to requests for comment.) 

Nevertheless, most scientists these days welcome the development of structured, or “spatially explicit,” models that account for the fact that any given member of a population is usually more closely related to individuals living nearby than to those living far away. 

Loosening our attachment to certain narratives of evolution can create space for wonder at the sheer complexity of life’s history.

Other scientists also say that random mating isn’t the only assumption in population genetics that merits scrutiny. Models rarely factor in natural selection, which can also create genetic patterns that look like hybridization. Another common assumption is that everyone’s DNA mutates at the same, constant rate. “All the theory says the mutation rate is fixed,” says Amos, the Cambridge population geneticist. But he thinks that rate would have slowed drastically in the group of Homo sapiens that expanded to Europe around 45,000 years ago. This, too, could have created genomic patterns that other scientists interpret as evidence of interbreeding with Neanderthals. 

phone with dna testing results and a cartoon neanderthal that says, "Hey Eric! You have more Neanderthal DNA than 96% of other customers."
Commercial genetic testing companies like 23andMe started offering customers Neanderthal ancestry reports.
COURTESY OF 23ANDME

The point here isn’t that a complex model of evolution with many moving pieces is necessarily better than a simple one. Scientists need to reduce complexity in order to see the underlying processes more clearly. But simple models require assumptions, and scientists need to reevaluate those assumptions in light of what they learn. “As you get more data, you can justify more complex models of the world,” says Mark Thomas, a population geneticist at University College London, who wrote a history of random mating in population genetics that highlighted how the field was starting to see it as “a limiting assumption as opposed to a simplifying one.” 

It can feel discouraging to couch conversations about the past in confusing terms like “population structure” and “mutation rates.” It seems almost antithetical to the spirit of science to talk more about uncertainty at the same time we are developing powerful technologies and enormous data sets for analyzing evolution. These tools often yield novel answers, but they can also limit the questions we ask. The French archaeologist Ludovic Slimak, for example, has complained that the idea of the inner Neanderthal has domesticated our image of Neanderthals and made it difficult to imagine their humanity as distinct from our own. Investigating Neanderthal DNA is sexier to many young researchers than searching for archaeological and fossil evidence of how Neanderthals actually lived. 

Loosening our attachment to certain narratives of evolution can create space for wonder at the sheer complexity of life’s history. Ultimately, that’s what Chikhi and Tournebize hope to do. After all, they don’t believe the question of population structure versus hybridization is either-or. It’s possible, and even likely, that both played a role in human evolution. “Our structured model does not necessarily mean that no admixture ever took place,” Chikhi and Tournebize wrote in their study. “What our results suggest is that, if admixture ever occurred, it is currently hard to identify using existing methods.” 

Future methods might disentangle the different factors, but it’s just as important, Chikhi says, for scientists to be up-front about their assumptions and test alternatives. “There’s still so much uncertainty on so many aspects of the demographic history of Neanderthals and Homo sapiens,” he notes. 

Keep that in mind the next time you read about your inner Neanderthal. The association between this DNA and some diseases may be real, of course—but would journals publish these studies without the additional claim that the DNA is from Neanderthals? Any good storyteller knows that sex sells, even in science. 

Ben Crair is a science and travel writer based in Berlin.