TGF-β1 has been deemed to serve as the predominant mediator of the pathology of renal fibrosis, whereas interferon-γ (IFN-γ), hepatocyte growth factor (HGF) and bone morphogenetic protein 7 (BMP-7) inhibit the production of matrix components primarily by counteracting TGF-β1 action [47,48,49,50,51,52,53]. This evidence concerns the gene TGFB1 and renal fibrosis.