This heterogenous association appears counterintuitive given that TP53 mutations confer a dismal prognosis in MDS and AML, and it is likely to be a product of the multitude of confounding factors modulating the behavior and fitness of TP53-mutated clones, such as previous exposure to cytotoxic chemotherapy (128), presence of germline pathogenic variants (Li-Fraumeni syndrome) (149), biallelic TP53 loss (150, 151), and mutation type (with missense variants behaving in a dominant-negative manner) (125). This evidence concerns the gene TP53 and acute myeloid leukemia.