The proapoptotic function of BAD is negatively regulated through phosphorylation by Akt, where upstream activation of Akt leads to inhibitory BAD phosphorylation at Ser136 and subsequent 14‐3‐3 sequestration.21 Since PTEN is frequently deleted in advanced prostate cancer, and results in constitutive activation of the PI3K/Akt pathway, we hypothesized that inhibition of BAD by Akt is a potential apoptosis evasion mechanism in prostate tumors. This evidence concerns the gene AKT1 and Familial prostate cancer.