Subsequent studies explored PTOV1 immunoreactivity in diverse PCa-related cases and found that PTOV1 expression increased from normal-looking epithelium (NEp) of the transition zone (TZ) through atypical adenomatous hyperplasia (AAH) and high-grade prostatic intraepithelial neoplasia (HGPIN) to PCa, suggesting its role in prostatic carcinogenesis [11–13]. This evidence concerns the gene PTOV1 and posterior cortical atrophy.