Since AT1aR and ACE are abundant in renal proximal tubule cells (PTCs), the present study used an inducible PTC-specific genetic mouse strain to delete either AT1aR or ACE in PTCs and determined whether deleting either component affects hypercholesterolemia-induced atherosclerosis in LDL receptor −/− mice. The gene discussed is LDLR; the disease is Hypercholesterolemia.