Considering the association between SIRT7, DSB DNA damage repair, and p53 regulation (Vakhrusheva et al., 2008), we hypothesize that p53 activation may contribute to the death of Sirt7−/− embryos and that deleting the p53 gene could alleviate this phenotype, albeit with increased genome instability and cancer risk in adulthood. The gene discussed is TP53; the disease is cancer.