Clinical studies also support the causal link between the circulating MCP-1 levels during obesity and the risk of stroke, coronary artery disease and plaque vulnerability implicated in atherosclerosis, due to the enhanced monocyte adhesion to the endothelium and the combination of macrophages with accumulated oxidized low-density lipoproteins (LDL), leading to the formation of foam cells and atherosclerotic plaques [105,106,107,108]. This evidence concerns the gene CCL2 and atherosclerosis.