Indeed, insights into the molecular pathobiology of AML have helped identify therapeutic targets and develop novel specifically tailored treatments toward multiple subsets of AML [31,32,33,34,35,36], including several mutation-specific tailored therapies, such as inhibitors of Fms-like tyrosine kinase 3 (FLT3) [38] and isocitrate dehydrogenase (IDH) [39,40]; glasdegib [41], an inhibitor of the hedgehog signaling pathway; and B cell leukemia/lymphoma 2 (BCL-2) inhibitors, such as venetoclax [42,43]. This evidence concerns the gene BCL2 and acute myeloid leukemia.