CDKN2A and acute myeloid leukemia: According to prior studies (41, 44, 45), TP53 mutations were remarkably higher in t-AML compared with de novo AML but presented lower rate of driver mutations such as NPM1 and DNMT3A. Furthermore, TP53 mutations seem to be mutually exclusive with other gene mutations such as NPM1, FLT3, ARF, and MDM2 (58).