Finally, our sequencing of t-AML/t-MDS suggests that the leukemogenic potential of expanded hematopoietic clones is strongly dependent on the specific mutations they harbor with TP53 mutant clones having a higher propensity towards leukemic evolution than clones with mutations in other DNA damage response genes, including PPM1D. In contrast to our findings, Lindsley et al. identified a high frequency (15%) of PPM1D mutations in t-MDS39. This evidence concerns the gene TP53 and myelodysplastic syndrome.