Thus, Nox4 deficiency abrogated HFD-induced atherosclerotic lesion formations as well as rFliC-mediated atherosclerosis including infiltration of monocyte and neutrophil, accumulation of collagen, and migration of VSMCs in ApoE KO mice indicating that Nox4 is an important mediator in the development of atherosclerosis. Here, APOE is linked to atherosclerosis.