KATs in the MYST: A New Therapeutic Vulnerability for SETBP1 -Mutated Myeloid Malignancies

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. XX .