A mechanistic study, using PC3 prostate cancer cells with active p53, or PC3 prostate cancer cells regardless of p53 status, demonstrated that SIRT1 inhibition by SIRT1 shRNA or sirtinol downregulates the deacetylation of p53 and FOXO1, thereby activating antiproliferative responses, such as apoptosis and senescence [86]. The gene discussed is TP53; the disease is prostate carcinoma.