AML is prone to relapse and drug resistance, which may be due to mutations in genes associated with epigenetic modifications (TET2, IDH1 and IDH2, DNMT3A, ASXL1, WT1, EZH2), genes associated with dysregulation of DNA repair (TP53, NPM1), and genes associated with defects in cell cycle inhibition and differentiation (NPM1, CEBPA, TP53, and GATA2). Here, TP53 is linked to acute myeloid leukemia.