Many leukocytes and inflammatory mediators are associated with the pathogenesis of AAA, including interleukin (IL)-1,−17, transforming growth factor (TGF)-β, and angiotensin II (AngII), which can infiltrate into aortic media and lead to smooth muscle cell depletion, generation of reactive oxygen species (ROS), and activation of matrix metalloproteinases (MMPs) causing ECM fragmentation (4). The gene discussed is IL1B; the disease is triple-A syndrome.