Kopp et al. also related that increased levels of circulating TGF-β1 induced progressive renal disease characterized by mesangial expansion, accumulation of glomerular immune deposits and matrix proteins, and interstitial fibrosis in this transgenic mouse model suggesting that chronically elevated circulating levels of TGF-β1 induce progressive glomerulosclerosis [15]. This evidence concerns the gene TGFB1 and kidney disorder.