Ku80−/− mice, which are defective in the repair of double-strand DNA breaks via the nonhomologous endjoining (NHEJ) pathway, are smaller than control littermates from embryonic day 17.5 on [41] and display multiple symptoms of premature senescence including kyphosis, atrophic skin, hepatocellular degeneration, and reduced lifespan due to cancer and sepsis [42]. This evidence concerns the gene XRCC5 and cancer.