Consistent with the results from PC3 cells with ablation of ARID4B (Fig. 1d), expression or phosphorylation of the core regulators and downstream effectors of the PI3K-AKT pathway were reduced in prostates of PtenPC−/−Arid4bPC−/− mice (Fig. 4e), suggesting a mechanism by which ARID4B is required for executing actions that promote prostate cancer in the context of PTEN deficiency. This evidence concerns the gene AKT1 and prostate carcinoma.