TP53 and neoplasm: As such, p533KR/3KRXrcc4−/− mice were generated by crossing p533KR and XRCC4 DNA repair-impaired mutants, and here we show that p533KR/3KR mutant completely rescue the embryonic lethality caused by XRCC4 deficiency, and unlike p53−/− Xrcc4−/− mice, p533KR/3KR Xrcc4−/− mice show a strong resistance to tumor formation, but surprisingly, display the accelerated aging phenotypes.