Angiotensin II and AT1 receptor could be involved in the growth of androgen independent prostate cancer since we found the higher expression of AT1 receptor in prostate cancer tissue than in normal tissue. Angiotensin II directly and indirectly stimulates the growth of prostate cancer cells and stromal cells including angiogenic cells. ARBs experimentally inhibited the proliferation of cancer cells and angiogenesis. The administration of ARBs for castration resistant prostate cancer (CRPC) induced the decline of serum prostate specific antigen (PSA) and the improvement of performance status in cachexic CRPC patients. These results support the hypothesis that an intrinsic RAS exists in the prostate gland and it is likely that ARBs are useful molecular targeting agents for CRPC.