Thus activation of Akt signaling alone in the presence of PTEN is insufficient to induce prostate cancer although the deletion of Akt1 but not Akt2 (Akt1 is the predominant isoform found in mouse prostate) was sufficient to suppress the development of high-grade PIN lesions in PTEN+/- mice [54, 58]. The gene discussed is AKT1; the disease is prostate intraepithelial neoplasia.