The most prevalent genetic anomalies observed in PCa include point mutations in genes such as SPOP, FOXA1, and TP53, as well as copy number alterations (CNAs) in AR, MYC, RB1, PTEN, CHD1, and fusion genes associated with the ETS (E26 transformation-specific) family [10,11,12,13,14,15,16,17]. This evidence concerns the gene SPOP and posterior cortical atrophy.