For example, p300 and CREB-binding protein (CBP), by acetylating AR, increase its transcriptional activity [73], and its inhibition in pre-clinical and early clinical trials has shown to downregulate the AR-dependent transcriptional program, modulate the expression levels of several biomarker in CRPC biopsies and tumour growth in both castration-sensitive and castration-resistant prostate tumours [74,75]. This evidence concerns the gene AR and prostate neoplasm.