To date, specific inhibitors have now been developed and used in clinical practice for certain subtypes of AML for which there is a well-known oncogene at the centre of disease pathogenicity, such as promyelocytic leukemia/retinoic acid receptor-alpha (PML/RARα) and FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD), or AML patients with mutations in isocitrate dehydrogenase isozymes 1 or 2 (IDH1, IDH2) [7,8]. This evidence concerns the gene FLT3 and acute promyelocytic leukemia.