Accompanied by the upregulation of LOX-1, high-fat diet also increased the expressions of ICAM-1, VCAM-1, and p47phox in ApoE−/− mice, which were all reversed by Rosiglitazone treatment (Figures 1(e)–1(h)), suggesting that PPAR-γ activation might effectively suppress LOX-1 expression and prevent endothelial inflammation and oxidative injury during the development of atherosclerosis. This evidence concerns the gene NCF1 and atherosclerosis.