BCL2 and acute myeloid leukemia: 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].