Sep 30, 2026 —
Researchers at Boston Children’s Hospital and the Broad Institute, led by Vijay Sankaran, have identified a new regulatory pathway that activates fetal hemoglobin, which they call the BACH2-NRF2 axis. Reactivating fetal hemoglobin is the central strategy for treating sickle cell disease and beta-thalassemia.
The finding matters because it is independent of BCL11A, the target of the approved gene-editing therapy Casgevy. A second, separate lever on fetal hemoglobin could open the door to editing or drug approaches that are simpler or more broadly accessible than today’s options.
The work is a genome-wide meta-analysis, and translating a target into a therapy is a longer road, but fetal-hemoglobin reactivation already has a clinical track record.
