Are We Getting Close to Safe Heritable Gene Editing? Not Yet, But the Gap Is Narrowing

Are We Getting Close to Safe Heritable Gene Editing? Not Yet, But the Gap Is Narrowing

Published: June 7, 2026, 14:25 UTC

In 2018, the Chinese researcher He Jiankui announced that he had used CRISPR-Cas9 to edit the genomes of three babies, altering a gene called CCR5 in an attempt to make them resistant to HIV. The scientific world reacted with horror. The technique was crude, the ethics nonexistent, and the children may have been left with unintended mutations that could affect their health for life. He spent three years in prison.

Eight years later, a new preprint from Columbia University has rekindled the debate. Researchers led by developmental cell biologist Dieter Egli used a far more precise tool — base editing — to make single-letter changes in healthy human embryos. The results, posted on bioRxiv on June 1, raise a question that would have been unthinkable in 2018: are we approaching the point where heritable human genome editing could be safe enough to consider?

The short answer, according to every scientist interviewed about the work, is no. But the gap is narrowing.

The critical difference between what He Jiankui did and what Egli’s team has done is the tool itself.

First-generation CRISPR-Cas9 cuts both strands of the DNA double helix. The cell then repairs the break using its own machinery, which is error-prone and often introduces large deletions, rearrangements, or even loses entire chromosomes. In embryos, this is a disaster: the edit might succeed in some cells but not others, creating a mosaic of genetically different cells within the same individual. He Jiankui’s three children are widely believed to be mosaics.

Base editing, invented in 2016 by David Liu’s group at Harvard, works differently. It cuts only one strand of DNA and chemically converts one nucleotide base to another — cytosine to thymine, for example — without ever creating a double-strand break. This dramatically reduces the risk of large-scale chromosomal damage.

Egli’s team used base editing on healthy two-cell embryos donated by parents undergoing IVF. They targeted two genes: PCSK9, which regulates cholesterol levels and is a validated target for heart disease prevention, and HBG1/HBG2, which control fetal hemoglobin production and are relevant to sickle cell disease and thalassemia.

The results were mixed. Editing PCSK9 succeeded in approximately 75% of cells with no detectable off-target changes — a result the researchers describe as clean and efficient. Editing the hemoglobin genes worked only about 50% of the time and often introduced unwanted changes alongside the intended edit.

The Mosaicism Problem

That inconsistency gets to the heart of why heritable genome editing is not ready for clinical use.

For a somatic gene therapy — editing cells in an adult patient’s body — 20% efficiency can be enough to treat disease. For an embryo, the edit must work in every single cell, because a single edited cell gives rise to the entire human body. If only some cells are edited, the resulting person would be a mosaic, carrying a mix of edited and unedited cells in every organ.

“There is currently no way to verify that a gene-edited embryo is not a mosaic,” said Yale obstetrician-gynecologist Emre Seli, who called the Columbia work a “conceptual shift” in the field but emphasized its limits. A single cell biopsied from an eight-cell embryo might test clean, but that biopsy cannot detect mosaicism in the remaining cells.

Yale’s Emre Seli called the work a “conceptual shift.” But even if the technical barriers fall, the ethical ones remain formidable. UC Berkeley molecular biologist Fyodor Urnov described embryo editing as “a solution in search of a problem” — many couples at risk of passing on genetic diseases already have the option of IVF with preimplantation genetic testing (PGT), which allows them to select unaffected embryos without any editing at all.

The Regulatory Vacuum

There is no binding international treaty governing heritable human genome editing. The governance landscape is a patchwork:

  • United States: A Congressional rider blocks the FDA from reviewing any application involving heritable genetic changes, creating a de facto ban. Research on embryos is permitted but cannot receive NIH funding.
  • United Kingdom: Heritable editing for reproduction is strictly prohibited. Embryo research is permitted under license from the HFEA.
  • European Union: Strictly prohibited under the Oviedo Convention.
  • China: Clinical heritable editing is banned with criminal penalties since the 2018 scandal, but heavy state investment in embryo research continues.

In May 2025, a coalition of major scientific societies called for a 10-year moratorium on reproductive germline editing. The Columbia results, the researchers say, do not change that calculus.

The Slippery Slope

Stanford bioethicist Hank Greely warned that the falling cost of the technology creates a different kind of risk. “For relatively little money — a handful of millions — an affluent individual could set up an IVF-plus-editing lab,” he said. The risk is not responsible scientists, but rogue actors, fly-by-night clinics offering “enhanced” babies to wealthy clients in jurisdictions with weak regulation.

The counterargument, made by some researchers, is that the technology could eventually eliminate devastating inherited conditions like sickle cell disease, thalassemia, and familial hypercholesterolemia from family lines permanently. Somatic base editing has already saved lives in clinical trials for cholesterol treatment. Extending that success to the germline, proponents argue, would be a natural progression.

Others point to a potentially safer path: editing sperm or egg stem cells before fertilization, which would eliminate the mosaicism problem entirely. A startup backed by Sam Altman and Brian Armstrong claims to be making progress on lab-grown human sperm, though the work remains at an early stage.

The Verdict

The Columbia preprint represents real progress. It shows that base editing in healthy human embryos can work with no chromosomal damage — something that was demonstrably not true of the technique He Jiankui used. That the hemoglobin targets failed more often than the cholesterol target is an honest signal of where the field is: still learning which genes can be safely edited and which cannot.

But the fundamental barrier remains. Until researchers can guarantee that every cell in an embryo carries the intended edit and no others, heritable human genome editing will remain what it has always been: a technical possibility that the world is not ready to accept.

The gap is narrowing. It has not yet closed.


Key preprint: Stepan Jerabek, Jimin Kim, Julie Sung, et al. “Efficient base editing and development in human embryos without chromosomal alterations.” bioRxiv, June 1, 2026. DOI: [10.64898/2026.05.30.728989](https://doi.org/10.64898/2026.05.30.728989)

Lead institution: Columbia University, Department of Genetics and Development, New York

Note: this article draws on reporting by Michael Le Page in New Scientist (June 5, 2026) and direct analysis of the underlying preprint.

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