p53 limits the expansion of cells that have acquired potential tumorigenic mutations either by promoting cell cycle arrest and DNA repair or by inducing apoptosis of highly damaged cells.1 In addition, p53 controls numerous mechanisms allowing adaptation of cells to adverse conditions such as stimulation of anti-oxidant defenses, control of metabolism and autophagy, and several others.1 Consistent with its tumor-suppressive functions, inactivation of Trp53 increases spontaneous and carcinogens-induced tumorigenesis in mice. This evidence concerns the gene TP53 and neoplasm.