As another possible mechanism, the binding of PAI-1 to vitronectin is known to modulate cell-matrix adhesion, cell migration, and cell phenotype via its interaction with integrins or urokinase-type plasminogen activator receptor (u-PAR) [28–30] and a recent study indicates that the vitronectin-binding function of PAI is more important for the progression of pulmonary fibrosis than its anti-protease activity [31]. Here, VTN is linked to pulmonary fibrosis.