Deletion of Smad7 enhances renal fibrosis and inflammation, whereas, overexpression of Smad7 attenuates renal fibrosis and inflammation by blocking the activation of both TGF-β/Smad and nuclear factor-κB (NF-κB) signaling pathway in a variety of animal models with kidney diseases [14-22]. The gene discussed is NFKB1; the disease is renal fibrosis.