However, both patient data analysis and pre‐clinical animal model studies invariably show that loss of PTEN promotes enhanced AKT activity and reduced AR signaling and that inhibition of AKT results in AR activation while blockade of AR function increases AKT activities (Carver et al, 2011; Mulholland et al, 2011), stressing the requirement of co‐targeting of both pathways for effective treatment of prostate cancer. This evidence concerns the gene PTEN and prostate carcinoma.