The concomitant accumulation of p53, p21CDKN1A, and p16INK4a, together with the finding that proliferation arrest could be bypassed by inactivating the Rb and p53 pathways, promoted the concept that oncogene-induced senescence was a component of the DNA damage response (DDR) that evolved as a tumor suppression mechanism [5]. The gene discussed is TP53; the disease is neoplasm.