Li et al. [22] found that inhibition of PP1 and PP2A lead to higher activity of Akt with resulting increase of survival of prostate cancer cells while Facompre et al. [23] proposed that increased activity of Akt increases JARID1B levels which initiates further Akt activation by repressing PTEN and enhancing by this mechanism PI3K/Akt signaling. This evidence concerns the gene PTEN and prostate cancer.