Administration of anti-TGF-β antibodies (10 mg/kg, 2/week) to Ang II-infused C57BL/6 mice led to the development of AAA in 80% of the mice and 40% mortality from aneurysm rupture, and it abrogated serum TGF-β levels and the phosphorylation of SMAD-2 within the aortic wall62. The gene discussed is AGT; the disease is triple-A syndrome.