The consistently upregulated expression level of ARD1 protein detected in human PCa cell lines and prostate tumor tissue samples has been suggested to promote prostate tumorigenesis through a positive-feedback mechanism, where ARD1 gets upregulated and functionally activated by androgen in an AR-dependent manner and, in turn, positively regulates AR activity by interacting with AR and acetylating it to promote AR nuclear translocation (120, 121). This evidence concerns the gene AR and posterior cortical atrophy.