This is supported by many studies in which overexpressing renal Smad7 can block TGF-β/Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation in diabetic kidney disease 22, 118, crescentic glomerulonephritis 119, UUO 120, AKI 69, and hypertensive nephropathy 22, 120, 121. This evidence concerns the gene SMAD3 and inflammatory response.