Moreover, considering that CgA is a good substrate of thrombin and plasmin [24, 25], often present in tumors, and that PN-1 is a potent inhibitor of these proteases [38], it is tempting to speculate that PN-1 may also serve to prevent the local cleavage of CgA in tumors (thereby preserving its anti-angiogenic activity) and/or other factors necessary for tumor progression and invasion. Here, PLG is linked to neoplasm.