To examine the effect of CTLA-4 overexpression in T cells on the development of AAA, we established hypercholesterolemic CTLA-4-Tg/Apoe−/− mice expressing full-length CTLA-4 under the control of human CD2 promoter12 on atherosclerosis-prone background, and induced AAA by continuous angiotensin II infusion in these mice. This evidence concerns the gene AGT and triple-A syndrome.