Both early and delayed administration of CDDO-Me to experimental mice was able to inhibit the development of prostate adenocarcinoma and its distant metastasis; in vitro studies on TRAMPC-1 prostate cancer cells revealed the inhibition of the antiapoptotic p-AKT, p-mTOR and NFκB proteins thus indicating AKT as a potential in vivo target for CDDO-Me. Here, NFKB1 is linked to prostate cancer.