Our data strongly suggest that the development of 2K1C Goldblatt hypertension is not solely dependent on increased renin expression and renin release from the clipped kidney into the circulation, where Ang II induces 2K1C hypertension by activating AT1a receptors in other target tissues [10,12,13,15,16,17,22,45]. The gene discussed is AGT; the disease is hypertensive disorder.