A series of studies have provided crucial findings about the pathogenesis of AAA, including infiltration of lymphocytes and macrophages into the aneurysmal lesion, synthesis and excretion of inflammatory mediators and protease (especially matrix metalloproteinases, MMPs), degradation of elastin and collagen in the media and adventitia, apoptosis of vascular smooth muscle cells (VSMCs) induced by inflammatory response, as well as destruction of arterial wall and expansion of aortic lumen7. The gene discussed is ELN; the disease is triple-A syndrome.