This model of angiotensin II administration was shown to induce a complete endothelial dysfunction, including hypertension, vascular remodeling, prooxidant and proinflammatory activity (resulting in increased production of TNFα, IL-1β, IL-17A, IL-4, TGFβ, and IL-10 in the kidney, and systemic soluble VCAM, ROS, and ICAM-1 expression), and organ injury (Trejo-Moreno et al., 2021). The gene discussed is IL17A; the disease is endothelial dysfunction.