Various genetic and epigenetic mechanisms regulating the pathophysiology of AML have been identified many of which cluster in particular categories of genes including those coding for signaling molecules (such as FLT3 and KIT), transcription factors (such as CEBPA and RUNX1), chromatin modifiers (such as MLL and ASXL1) or direct and indirect regulators of DNA methylation (such as DNMT3A, IDH1, IDH2, and TET2) (7, 8). The gene discussed is FLT3; the disease is acute myeloid leukemia.