Interestingly, when the Cry1/2−/− mutation is combined with p53−/− mutation following a commonly used strategy to uncover the carcinogenicity of weakly penetrant tumorigenic genes, the opposite of the expected effect was found: the p53−/− mice developed lymphomas and lymphosarcomas and had an average lifespan of 5.5 months, whereas the p53−/−Cry1/2−/− mice developed tumors later and lived 1.5-fold longer than the p53−/− mice (42). The gene discussed is TP53; the disease is lymphoma.