For example, deficiency in any of the components of the MCP1/CCR2 proinflammatory axis (a main inflammatory pathway in the recruitment of monocyte-derived macrophages in atheroma lesions) in LDLr-/- or apoE-/- or in transgenic human apoB mouse models decreases atherosclerosis development despite high-cholesterol feeding [85]. Here, CCL2 is linked to atherosclerosis.