The importance of each AKT isoform in PTEN-deficient prostate cancer remains unclear, with some preclinical data suggesting a higher dependency on AKT2 compared to AKT1 [193], yet only deletion of Akt1 and not Akt2 has been shown to suppress prostate neoplasia in a Pten+/− transgenic mouse [194,195]. The gene discussed is PTEN; the disease is prostate carcinoma.