BCL2 and acute myeloid leukemia: Several novel agents acting through distinct molecular targets, identified in the pathophysiology of AML, are being investigated alone or combined with conventional chemotherapy, e.g. FLT3 inhibitors (midostaurin6, gilteritinib7), IDH1/2 inhibitors (ivosidenib8, enasidenib9,10), BCL-2 inhibitors (venetoclax11,12), and cyclin-dependent kinase (CDK) inhibitors (CDKi; alvocidib13–15 fadraciclib16), which cause cell cycle arrest and induce apoptosis (Figure 1).