As discussed above, the stimulation of the AT1R by Ang II increases the release of cytokines, IL-6, and NOXs from endothelial cells, results in the production of vasoconstrictor agents from VSMCs, and further leads to vascular remodeling (e.g., aortic wall thickening) and hypertension (e.g., pressure overload). The gene discussed is AGTR1; the disease is hypertensive disorder.