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. The gene discussed is SMAD3; the disease is inflammation.