A plethora of reports suggest that p21 protects the cells from stress or p53-dependent and p53-independent apoptosis, although the mechanisms are poorly understood.4, 5, 6, 7 Delayed treatment of cancer cells with genotoxic agents causes caspase-3-mediated p21 cleavage and subsequent inactivation, thereby triggering apoptosis.8 Moreover, p21 shields the cancer cells from death induced by DNA-damaging agents, and altered p21 expression increases sensitivity to treatment in vivo. This evidence concerns the gene CDKN1A and cancer.