First, Pin1 inhibition suppressed vascular inflammation and atherosclerosis as well as activation of NF-κB signaling in ApoE−/− mice; Second, Pin1 inhibition improved oxLDL-induced inflammatory response in endothelial cells; Third, Pin1 inhibition suppressed the activation of NF-κB and decreased endothelial cells activation induced by oxLDL, at least partly via NF-κB signaling. This evidence concerns the gene NFKB1 and atherosclerosis.