During the progression to castration-resistant prostate cancer (CRPC), coactivators such as SRC-1 and TIF-2 greatly contribute to the growth of androgen-independent prostate cancer cells by reactivation of AR by coactivators which are highly overexpressed in recurrent prostate cancer compared with benign prostatic hyperplasia or androgen-dependent prostate cancer [28]. This evidence concerns the gene AR and prostate cancer.