Specifically we showed that SINT1 1) directly binds AF-1, 2) inhibited forskolin-induced transactivation of AR NTD, 3) attenuated transcriptional activities of both FL-AR and AR splice variant, 4) decreased FL-AR- and AR-V7-dependent proliferation of prostate cancer cells, and 5) in vivo decreased the growth of CRPC tumors concomitant with decreased serum levels and expression of PSA, a clinically relevant AR-regulated gene. The gene discussed is AR; the disease is prostate cancer.