For example, KAT2A activity sustains transcriptional networks supporting LSC survival and tumorigenicity in AML without impacting HSCs.144 KAT2A also promotes AML development by increasing the expression of MYC and modulating its transcriptional functions.149 Accordingly, KAT2A loss drives shrinkage in the LSC compartment by limiting self-renewal while promoting differentiation and inducing apoptosis, impairing AML progression overall.144,149. Here, KAT2A is linked to acute myeloid leukemia.