Based on the premise that concurrent loss of 2 or more tumor suppressor genes including PTEN, P53, and RB1 is associated with more aggressive metastatic PCa (31, 32), and P53 loss and RB1 loss are often late events first noted in castration-resistant disease, we asked whether an alternate route of phenotypic plasticity could be activated in the context of PTEN loss and potentially independent of P53 and RB1 loss. The gene discussed is PTEN; the disease is posterior cortical atrophy.