The RANTES leads to endothelial dysfunction of vascular inflammatory cell recruitment, atherosclerotic plaque and neointima formation.[41,42] RANTES is preserved in α-granules of the platelets and aggregates on the damaged EC surface after platelet activation, promoting the atherogenic recruitment of monocytes, which may aggregate the development of atherosclerotic plaque.[43]. This evidence concerns the gene CCL5 and endothelial dysfunction.