Renal fibrosis essentially evolves from inflammatory cell infiltration, and activated inflammatory cells not only produce several proinflammatory cytokines and chemokines such as chemokine ligand 2 (CCL-2)/monocyte chemotactic protein-1 (MCP-1) but also produce profibrotic cytokines like TGF-β1, which are regarded as major mediators in renal fibrosis pathogenesis [10]. Here, TGFB1 is linked to renal fibrosis.