Interestingly, uPA/uPAR, through the activation of the plasminogen system, degrade ECM, and consequently drive tumor cell membrane protrusion and motility.17 The RNAseq profiling for both PCa cells overexpressing HO-1 pharmacologically or genetically showed a direct regulation of the critical factors 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: CPB2 (thrombin activator of fibrinolysis inhibitor), SERPINF2 (alpha 2 anti-plasmin, and F12 (factor XIIA). The gene discussed is CPB2; the disease is posterior cortical atrophy.