AKT1 and prostate intraepithelial neoplasia: Elegant in vivo genetically-engineered mouse models have shown that heterozygous or homozygous deletion of PTEN in the prostate epithelium [4] or alternatively, constitutive activation of the downstream effector PKB/Akt [5] underpins the development of a prostate pathology recapitulating human prostatic intra-epithelial neoplasia (PIN), a pre-malignant condition.