AGT and triple-A syndrome: Interestingly, although a previous study identified that the vessel wall-resident but not bone marrow-derived AT1a receptor mediates AAA formation,43 recent data from cell-specific AT1a-knockout mice suggest that AT1a deficiency in vascular endothelial cells, VSMCs or adventitial fibroblasts alone does not affect AngII-induced aortic pathologies, such as AAA, atherosclerosis and medial hyperplasia of descending aortas.66,67 These findings indicate a potential synergistic effect between different vascular cell types during overactivation of AT1a receptor signaling in disease states.