In this study, we report several new findings: i) differential activation of PP-1 and Akt by MAB is determined by the genetic backgrounds of prostate cancer cells, and thereby controls AR-v7 protein stability; ii) PP-1 targets pSer(213) of AR-v7, prevents Mdm2 recruitment and Mdm2-mediated AR-v7 protein degradation by ubiquitin-proteasome pathway; and iii) Akt signaling regulates AR-v7 protein expression. Here, CD101 is linked to prostate carcinoma.