BCL2 and acute myeloid leukemia: The compounds that met our criteria, I-BET151, sunitinib, and quinacrine, rely on different mechanisms of action; however, they all converge in deregulating BCL-2 family proteins, revealing that KMT2A-r AML involved antiapoptotic factors and thus their targeting as a strategy to trigger their death, even more when combined with BCL-2 inhibitor venetoclax.