Several other pro-inflammatory molecules have been associated with endothelial dysfunction, such as IL-6, TNF-α, monocyte chemoattractant protein 1 (MCP-1), receptor for advance glycation endproducts (RAGE) and the pro-oxidant enzyme NADPH oxidase, and all predispose the vasculature to a “proatherogenic” phenotype [28,29,30]. This evidence concerns the gene CCL2 and endothelial dysfunction.