In their mouse model of AAN, Dai and co-workers showed that the loss of SMAD7 was associated with activation of TGF-β/Smad3 and NF-κB signaling pathways, resulting in aggravation of progressive fibrosis and inflammation in mice treated with AA, and that restoration of SMAD7 locally in the kidneys of Smad7 knockout mice inactivated TGF-β/Smad3-mediated renal fibrosis and NF-κB-driven renal inflammation, thereby preventing the progression of chronic AAN [100]. The gene discussed is SMAD3; the disease is Balkan nephropathy.