Second, mice with endothelial-specific insulin resistance that were also deficient in Nox2 and on an apolipoprotein E (ApoE)-deficient background develop increased lipid deposition in the thoraco-abdominal aorta, significant elastin fragmentation at the level of the aortic sinus, and increased expression of the adhesion molecule ICAM-1, despite reduced superoxide generation from endothelial cells and enhanced endothelial-dependent vasorelaxation. Here, APOE is linked to Insulin resistance.