To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression. This evidence concerns the gene TP53 and prostate adenocarcinoma.