In the present study, using hypercholesterolemic mice constitutively expressing T-cell coinhibitory molecule CTLA-4, which is known to play a critical role for negatively regulating T cell immune responses, in T cells, we have clearly demonstrated, for the first time to our knowledge, that CTLA-4 overexpression in T cells effectively prevents AAA formation by suppressing systemic and aortic immunoinflammatory responses in angiotensin II-infused hypercholesterolemic mice. This evidence concerns the gene CTLA4 and triple-A syndrome.