In this study, we used siRNA and lentiviral vector technology to knock down TAB1 in HG-induced macrophages and STZ-induced diabetic mice, then evaluated glycolysis, polarization of macrophages and levels of inflammation, thereby exploring the relationship between the TAB1/NF-κB/HIF-1α signaling pathway and glycolysis in polarization of macrophages in the DN microenvironment. The gene discussed is NFKB1; the disease is liver dysplastic nodule.