Animal studies in the Ang II–induced model of hypertension showed that cell-specific CypD knockout in endothelial cells prevents vascular oxidative stress, preserves endothelial-dependent relaxation, protects endothelial nitric oxide production, and attenuates Ang II–induced vascular hyperpermeability, indicating that endothelial CypD depletion protects the endothelial function (Figures 1 and 3). Here, AGT is linked to Hypertension.