Indeed, previous studies also indicated the roles of uPAR in attenuating myofibroblast functions, and these included proliferation, recruitment, and the subsequent progression of renal fibrosis by regulating extracellular signal-regulated kinase (ERK) signaling and reducing the extracellular accumulation of PAI-1 [36], which are also well-documented downstream targets of TGF-β1 signaling [11,37,38]. Here, TGFB1 is linked to renal fibrosis.