It can activate the NF-κB signaling pathway by targeting the inhibition of SOCS-1, leading to the phenotype polarization of M1 macrophages, further increasing the expression of MCP-1, IL-1β, and other renal inflammatory cytokines, and promoting the occurrence of renal tubulointerstitial inflammation in diabetic nephropathy (81). The gene discussed is CCL2; the disease is diabetic kidney disease.