Our results unveiled that when PCa cells overexpressed HO-1 there was a direct transcriptional regulation of the critical players in the uPA/uPAR cascade, such as the downregulation of the axis activators: uPA/uPAR (PLAU/PLAUR) and tPA (PLAT), and the upregulation of the axis inhibitors: thrombin activator of fibrinolysis inhibitor (CPB2), alpha 2 anti-plasmin, (SERPINF2) and Factor XIIA (F12) (Figure 3A, left panel) [16]. This evidence concerns the gene CPB2 and posterior cortical atrophy.