The development of renal fibrosis is generally considered to result from maladaptive repair processes induced by the release of a variety of profibrotic factors such as transforming growth factor-beta (TGF-β), in which infiltrating inflammatory cells including macrophages, stimulate the formation of myofibroblasts via the differentiation from tissue-resident fibroblasts and bone marrow-derived mesenchymal stem cells (MSCs), and epithelial-to-mesenchymal transition (EMT). The gene discussed is TGFB1; the disease is renal fibrosis.