The precise reason for the disproportionate prevalence of TP53 gene mutations in del(5q) MDS is unknown, but one could speculate that mutant clones may be selected for under the pressure of constitutive activation of this pathway in this particular cytogenetic MDS subset, analogous to other cancers in which such mutations emerge in the presence of ongoing cellular stress or DNA-damage response activation (46). This evidence concerns the gene TP53 and myelodysplastic syndrome.