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). The gene discussed is NAA10; the disease is posterior cortical atrophy.