The results indicated that knockdown of TRAF3IP2 inhibited high glucose-induced IKKβ and JNK phosphorylation; inhibited p65 and c-Jun nuclear translocation; and inhibited the expression of NF-κB-dependent proinflammatory cytokines, chemokines, and adhesion molecules, thereby contributing to the alleviation of endothelial dysfunction and a reduction in the risk of atherosclerosis. The gene discussed is JUN; the disease is endothelial dysfunction.