TP53 and acute myeloid leukemia: Contrariwise, mutations involving triggered signaling pathways (i.e. FLT3, RAS, PTPN11, BCOR, JAK2, NF1) and polycomb mechanisms (i.e. SF3B1, KDM6A, SRSF2) frequently occurred in sub-clones, indicating that these alterations may productively stimulate TP53 AML throughout clonal evolution.