The clinical success of agents targeting the PI3K/AKT/mTOR pathway could be maximized by prospectively identifying patients harboring molecular abnormalities in this pathway who may have a higher likelihood of responding, that is loss of PTEN demonstrated by FISH, high levels of AKT expression, and loss of p27 identified by immunohistochemistry in the patient's PCa tissue. Here, AKT1 is linked to posterior cortical atrophy.