KATs in the MYST: A New Therapeutic Vulnerability for SETBP1-Mutated Myeloid Malignancies
Mark Soto1,2, Kira Gritsman1,2,3
1Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York.
Blood Cancer Discovery
|June 1, 2026
Abstract:
Carlson and colleagues demonstrate that SETBP1 mutations promote leukemic self-renewal by recruiting MYST acetyltransferase complexes (KAT7/KAT6A) to chromatin, where H3K14ac and H3K23ac marks are deposited on promoter sites for key stemness genes. Genetic deletion or pharmacologic inhibition of KAT7/KAT6A was shown to shut down this SETBP1-associated self-renewal program and promote myeloid differentiation of SETBP1-mutant cells. See related article by Carlson et al., p. 606.


