Overall, findings presented, and combined with previous reports, clearly underscore the need to test rational MI-based combinations that would overcome escape mechanisms in AML controlled by epigenetic drivers such as BRD4 or HATs, e.g., by employing MI plus BETi or HATi; or by growth promoting signaling kinases such as CDK4/6 or FLT3, e.g., by MI plus abemaciclib or MI plus quizartinib; or by anti-apoptotic proteins such as BCL2, e.g., by combining MI with venetoclax [18, 57]. The gene discussed is BRD4; the disease is acute myeloid leukemia.