We previously showed that renal Smad7 is lost in streptozotocin (STZ)-induced diabetic kidneys, which is associated with enhanced renal fibrosis and inflammation by activating the TGF-β/Smad3 and NF-κB signaling pathways, whereas the overexpression of Smad7 in diabetic kidneys attenuates TGF-β/Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation 14. The gene discussed is SMAD3; the disease is renal fibrosis.