Several AR-related mechanisms have been proposed for metastatic or androgen-independent PCa progression including: 1) AR amplification, 2) a hypersensitive AR resulting from point mutations, 3) promiscuous mutant-AR protein activated by non-androgenic ligands and 4) AR-polymorphisms changing the response to androgen (e.g., poly-CAG repeat). This evidence concerns the gene AR and posterior cortical atrophy.