For instance senescent cells with low expression of tumor suppressor p16ink4 resume cell growth upon inactivation of tumor suppressor p53 [46], p53 null lung cancer cells escape senescence induced by various drugs including cisplatin, camptothecin, etoposide, paclitaxel and vindesine by upregulating cyclin-dependent kinase 1 (Cdk1) [47], senescent colon and breast cancer cells regain proliferative capacity upon exposure to doxorubicin [48, 49], whereas senescent melanoma cells proliferate again upon the overexpression of the inhibitor of apoptosis protein survivin [50]. Here, TP53 is linked to melanoma.