The main oncogenic signaling pathway implicated at this juncture is the PI3K/AKT-pathway, predominantly activated through frequent functional loss of the inhibitory tumor suppressor phosphatase and tensin homolog (PTEN), which is less common in localized PCa (20–30%) but becomes more dominant and is found in up to 50–60% of mCRPCs. This evidence concerns the gene AKT1 and posterior cortical atrophy.