Although one prevailing hypothesis has been that the RAS in circulating leukocytes and/or resident cell types of the vessel wall exerts an important role in atherosclerosis (5–9), deletion of AT1aR on macrophages (a major cell type in atherosclerosis) or resident cell types of the arterial wall does not affect atherosclerosis (9–11), indicating that AngII-AT1aR stimulation may not act directly on the vascular wall to promote atherosclerosis. The gene discussed is AGT; the disease is atherosclerosis.