Given the multiple roles of this master suppressor in controlling anti-proliferative responses encompassing cell cycle arrest, apoptosis, differentiation, senescence, DNA repair, metabolism and immune response [5], the low frequency of somatic TP53 mutations in BCP-ALL raises the question whether the p53 pathway might be functionally impaired by mechanisms other than mutations in these neoplasms. This evidence concerns the gene TP53 and acute lymphoblastic leukemia.