Some of the AR-based hypotheses to explain the development of ADI disease include development of activating AR mutations [10], AR activation by testosterone and dihydrotestosterone, which can be present in recurrent prostate cancer tissue at levels sufficient to stimulate AR [11], AR activation by a pool of ligands generated intraprostatically by increased expression of genes regulating androgen metabolism [12], or even AR activation by anti-androgens [13]. The gene discussed is AR; the disease is prostate carcinoma.