There is evidence of preleukemia driven by early mutations such as DNA methyltransferase 3A, methylcytosine dioxygenases TET1 and TET2, isocitrate dehydrogenase 1 (IDH1) and IDH2, and TP53 (which encodes p53); whereas late mutations such as FMS-like tyrosine kinase-3 (FLT3) or KRAS promote proliferation, block differentiation, and drive the progression of AML.27 The gene discussed is TP53; the disease is acute myeloid leukemia.