Since Smad7 functions as an integrated inhibitor for both TGF-β/Smad–signaling and NF-κB–signaling pathways, once renal Smad7 is degraded, TGF-β/Smad and NF-κB signaling becomes activated, resulting in the development of renal fibrosis and inflammation [74]. The gene discussed is NFKB1; the disease is renal fibrosis.