Their clinical sequencing analysis of PCa genomes has revealed that the majority of individuals with CRPCs harbor molecular alternations in the AR gene, as well as in genes encoding the main components of the WNT/β-catenin pathway, such as APC, β-catenin and R-spondins, leading to overactivation of WNT/β-catenin signaling [222]. The gene discussed is AR; the disease is posterior cortical atrophy.