NOTCH1 and posterior cortical atrophy: Abnormal expression of Notch receptors and ligands leads to Notch signaling dysfunction, which regulates tumor formation and progression in PCa as an oncogene or tumor suppressor gene.198 For example, previous studies have shown that local high-risk PCa and metastatic castration-resistant PCa cells express high levels of Notch1 receptors, and activated Notch1 cooperates with multiple carcinogenic pathways to drive the invasiveness of PCa.199