In line with this finding, the present study added new evidence that the development of renal inflammation in chronic AAN was associated with a marked activation of NF-κB signaling, which was negatively regulated by Smad7 because deletion of Smad7 enhanced but restored renal Smad7 in Smad7 KO mice or overexpression of Smad7 in the diseased WT mice inhibited NF-κB-mediated renal inflammation including upregulation of TNFα, MCP-1, and infiltration of macrophages and T cells in chronic AAN. The gene discussed is SMAD7; the disease is Balkan nephropathy.