One interpretation of this data is that accelerated cell cycle entry, or proliferation as indicated by the incidence of mitotic figures and Ki67 staining contributed by Rb1G (Fig 2C), contributes to cancer susceptibility in Trp53-/- mutants because it complements a DNA damage-induced cell cycle arrest defect, or other cancer relevant deficiency, that is inherent to Trp53 knock outs. This evidence concerns the gene TP53 and cancer.