Preclinical studies have demonstrated that administration of P2Y12 inhibitors attenuates endothelial dysfunction via reducing the expression of inflammatory molecules (including vascular cell adhesion molecule-1), macrophage accumulation, and lipid deposition whilst ameliorating the impairment of endothelium-dependent vasodilation by adenosine diphosphate via decreased phosphorylation of the JNK [67]. This evidence concerns the gene P2RY12 and endothelial dysfunction.