Since the endothelial dysfunction denotes the initiation of atherosclerosis, enhanced inflammation promotes the development of vulnerable plaques, and reactive oxygen species (ROS) exert harmful effects such as the induction of the apoptosis of macrophage and smooth muscle cells [4], [5], the blockade of the AT1 receptor may suppress atherosclerosis progression and stabilize vulnerable plaques. This evidence concerns the gene AGTR1 and endothelial dysfunction.