What happened
A team from University Hospital Tubingen and Columbia, including Michel Sadelain and Judith Feucht, traced a big part of that exhaustion to a single protein: NFIL3. When they used CRISPR to switch it off, the CAR T-cells stayed functional longer and fought tumors more effectively.
This is the kind of finding that quietly moves a whole field. The promise of cell therapy has always been limited by durability. If you can target one regulator to keep engineered immune cells in the fight, you widen the set of patients these therapies can actually help.
It is early, and a CRISPR edit in the lab is not a clinic-ready product. But the logic is exactly right: stop accepting exhaustion as inevitable and engineer around it. Curious what the cell-therapy people here think about NFIL3 as a target.
Source
Reported by A single protein may be holding back CAR T cancer therapy via sciencedaily.com, published June 2, 2026.