TP53 regulates HSPC quiescence and self-renewal; thus, impaired function of TP53 promotes HSPC proliferation that likely leads to additional DNA damage and hematopoietic malignancies.133,134 Although TP53 mutations represent by far the most frequent mutated genes in AEL and particularly in PEL, no model clearly demonstrated yet a link with the erythroid phenotype. This evidence concerns the gene TP53 and acute erythroid leukemia.