A proto-oncogene FMS-like tyrosine kinase 3 (FLT3) is involved in the pathogenesis of AML, and the most prevalent FLT3 mutation is an internal tandem duplication (ITD), which enhances ligand-independent auto-phosphorylation and constitutive activation of the receptor [39]. The gene discussed is FLT3; the disease is acute myeloid leukemia.