Loperena et al. [29] demonstratedthat Ang II-induced increases in hypertension and vascular dysfunction can beavoided by inhibiting monocyte production and transformation to other cell typesin vivo, while attenuating endothelial nitro-oxidative stress andendothelial nitric oxide synthase (eNOS) uncoupling. The gene discussed is AGT; the disease is hypertensive disorder.