An important therapeutic strategy in AML is the combination of venetoclax (a BH3-mimetic that blocks the anti-apoptotic BCL-2, frequently overexpressed in AML, reviewed in [108]) with low-doses of cytarabine or decitabine or azacitidine in previously untreated patients older than 65 years [109]. The gene discussed is BCL2; the disease is acute myeloid leukemia.