Cerebral circulation has been extensively studied under the pathophysiological conditions of ischemia and reperfusion; in particular, previous data obtained using in vitro models indicate that angiotensin II (Ang II) affects cerebral microcirculation through the activation of angiotensin II Type 1 receptor (AT1R) during ischemia–reperfusion injury [1,2,3,4]. The gene discussed is AGT; the disease is ischemia.