According to recent reports, both, TP53 mutated AML and MDS-EB-2, have practically undistinguishable biology; have blast count 15%-20% (20% cutoff is not considered specific any longer), in the majority (50%—70%), have no co-existing driver mutations or rareness of NPM1 or FLT3 alterations [24, 43], and possess high incidence of complex/monosomal karyotypes (80%–90%), which include abnormalities in chromosomes 5, 7, and 17 [24]. Here, TP53 is linked to acute myeloid leukemia.