Upregulation of the serine protease inhibitor PAI-1, in tumor cells, in mesenchymal cells within the tumor microenvironment as well as by “wound-stimulated” epithelial cells, may subsequently shift this proteolytic balance to optimize creation of a migratory “scaffold.” The available data clearly implicate PAI-1 as a major upstream modulator of a uPA→plasmin-generating system that exerts fine control over the MMP-dependent pericellular proteolytic cascade. Here, SERPINE1 is linked to neoplasm.