As an exemplar of this principle, we and others have recently shown the efficacy and mechanism of action of protein–protein interaction inhibitors of the bromodomain and extra-terminal (BET) family of epigenetic readers in animal models of mixed lineage leukemia (MLL)-rearranged leukemias,6, 7 multiple myeloma8 and non-Hodgkins lymphoma.9 However, the efficacy and potential mechanism(s) of action of BET inhibitors in other forms of AML are largely unknown. The gene discussed is KMT2A; the disease is acute myeloid leukemia.