Collectively, these studies show that the mechanisms by which dysfunctional ECs drive AAA formation are diverse, ranging from decreased NO production/eNOS uncoupling to a phenotypic switch that results in a pro-thrombotic, pro-inflammatory state with differing distributions of EC sub-populations in the setting of pathologic biomechanical stresses in aneurysm prone regions (Figure 1). The gene discussed is NOS3; the disease is aneurysm.