On Sept. 5, 2025, in a medical first, researchers report that they have implanted CRISPR-edited pancreas cells into a person with type 1 diabetes. The cells pumped out sugar-regulating insulin for months — without the need for the recipient to take immune-dampening drugs, thanks to gene edits that allowed the cells, collected from a deceased donor, to evade detection by the recipient’s immune system.

The study, orchestrated by the firm Sana Biotechnology in Seattle, Washington, raises hopes of an enduring cure for an autoimmune disease that consigns millions of people to a life of strict monitoring and dependence on injected insulin. “The preliminary data has definitely lifted the spirits of our community — and it’s a really elegant approach,” says Aaron Kowalski, chief executive of Breakthrough T1D, a non-profit organization in New York City formerly known as JDRF.

The ultimate goal is to apply immune-cloaking gene edits to stem cells and then direct their development into insulin-secreting islet cells. Unedited islets made from stem cells have already shown promise for treating type 1 diabetes in a small trial, according to results published in June.

Currently, the only way for someone with type 1 diabetes to avoid dependence on injected insulin is through the transplantation of cadaveric islet cells. The procedure can restore insulin production for years, but it is rarely performed — constrained by the scarcity of donor pancreases and the need for lifelong immune-suppressing drug therapy, which carries risks of infection, cancer and other serious side effects.

Sana’s strategy aims to bypass the need for those drugs entirely. Company scientists began with islets from a deceased donor who did not have diabetes. Using the CRISPR gene-editing system, the researchers disabled two genes that normally help to flag foreign invaders to T cells, the immune system’s front-line defender. They then used a virus to shuttle genetic instructions for a protein called CD47 into the cells. This protein serves as a protective ‘do not eat me’ signal that prevents immune watchdogs, known as natural killer cells, from attacking the edited cells