TP53 and lip and oral cavity carcinoma: Thus, like SIRT1, SIRT3 may bind and deacetylate Ku70, promoting Ku70-Bax interactions and attenuating apoptosis in cardiomyocytes.20 In addition, mitochondrial SIRT3 is required for Nampt, a stress and diet-responsive regulator of mitochondrial NAD+ levels, to promote cell survival during genotoxicity.21 More recently, it was reported that SIRT3 abrogates p53 activity, thus preventing growth arrest and senescence in bladder carcinoma cells.22 These findings suggest a role for SIRT3 in carcinogenesis; however, to our knowledge, the role of sirtuins has not been investigated in oral cancer.