Based on the previous observation that Rb1G/G; Trp53-/- mice have a shorter latency to tumor formation than Trp53-/- controls, and that Rb1G/G; Cdkn1b-/- mutations cause similar cell cycle control defects and are also cancer prone, we crossed Rb1G/G mice with p21 deficient animals. This evidence concerns the gene CDKN1A and cancer.