In summary, HAT1, a previously unrecognized regulator of AR, transcriptionally upregulates AR expression in PCa cells through a BRD4‐mediated pathway, and inhibition of HAT1 re‐sensitizes CRPC cells to ENZ treatment, suggesting that HAT1 serves as a critical oncoprotein and an ideal target for the treatment of ENZ‐resistant CRPC patients. Here, HAT1 is linked to posterior cortical atrophy.