Pathophysiological role of glycolytic switch in vascular smooth muscle cells promotes aortic aneurysms and vascular fibrosis,43, 44 and targeting of vascular glycolysis was proposed to reduce the aneurysmal formation and diminish mortality due to reduced aortic ruptures.45, 46 We have tested whether depletion of smooth muscle CypD reduces maladaptive switch to vascular glycolysis by lactate production in intact and denuded aortas isolated from sham and Ang II–induced SmcCypDKO and wild-type mice. The gene discussed is AGT; the disease is aortic aneurysm.