However, the pathological mechanisms underlying aneurysm formation in Marfan and non-Marfan patients, as well as in an angiotensin II (AngII)-infused ApoE−/− mouse model of AAAs [7], are similar and involve alterations in the ECM composition and structure, particularly affecting elastin and collagen fibers [8], which play an important role in providing the aortic wall with elasticity and tensile strength [9]. The gene discussed is AGT; the disease is aneurysm.