These pharmacological approaches include the BCL-2 inhibitor venetoclax [48], the CD33 monoclonal antibody gemtuzumab ozogamicin [49], and the hedgehog inhibitor glasdegib [50], in addition to agent-specific inhibition ofrecurrent AML mutated genes, namely FLT3 inhibitors, such as midostaurin [51], gilteritinib [52], and quizartinib [53], as well as the IDH1 and IDH2 inhibitors ivosidenib and enasidenib [54,55], respectively. This evidence concerns the gene FLT3 and acute myeloid leukemia.