AKT1 and posterior cortical atrophy: A previous study from our laboratory demonstrated that although Akt1 is essential for oncogenic transformation in a neuroendocrine PCa TRAMP mouse model, pharmacological inhibition of Akt using triciribine in advanced PCa bearing TRAMP mice or genetic ablation of Akt1 gene in PC3 and DU145 human PCa cells augmented EMT and metastasis [13].