The compound was also investigated on the hormone-refractory PC-3 (AR-) and C4-2 (AR+) prostate cancer cell lines where it strongly inhibited cell proliferation and induced apoptosis, when applied in very low concentrations; in terms of molecular mechanism, CDDO-Me inhibited p-AKT, mTOR and NF-kB signaling proteins and, consequently, their downstream targets. This evidence concerns the gene AKT1 and prostate carcinoma.