Indeed, this is supported by our recent studies showing that proximal tubule-specific deletion of AT1a receptors or NHE3 in the kidney not only lowers basal blood pressure by inhibiting proximal tubule Na+ reabsorption and promoting the pressure-natriuresis response, but also markedly attenuated Ang II-induced hypertension in PT-Agtr1a−/− or PT-Nhe3−/− mice [32,33,34,35,57,58]. The gene discussed is SLC9A3; the disease is Hypertension.