This is not surprising considering (1) that hypertension had already developed before knockout induction, (2) that angiotensin II–induced contraction was similar in control and Y/T KO at 11 days, and (3) that angiotensin II–induced hypertension in mice may primarily be due to smooth muscle–independent effects, such as increased fluid retention.17 The resulting increase in blood pressure combined with defective adaptive mechanisms in Y/T KO mice is likely contributing to elevated wall stress and lesion development in small arteries. The gene discussed is AGT; the disease is hypertensive disorder.