During glomerular disease progression, NF-κB activation triggers an inflammatory cascade that produces inflammatory factors, such as IL-10 and MCP-1.Studies have found (186) that TGF-β/SMAD and NF-κB signaling pathways play an important role in HTN, and SMAD7, as a downstream inhibitor of these two pathways, can inhibit proteinuria and serum creatinine, and improve glomerular filtration rate, thereby alleviating the condition of HTN. This evidence concerns the gene IL10 and hypertensive disorder.