Hormone therapy in prostate cancer implies the inhibition of androgen action in cancer cells by the systemic ablation of androgens through castration (medical or surgical), or by ARAT, which entails either inactivation of the AR due to its binding to an antagonist or suppression of intratumoral androgen biosynthesis by inactivating CYP17A1, a cytochrome P450 enzyme that catalyzes a rate limiting step in the steroidogenic pathway to testosterone and DHT production. This evidence concerns the gene AR and prostate cancer.