Our findings of attenuated Teff immune responses and AAA development mediated by CTLA-4 overexpression does not appear to be due to modulation of Treg responses, because angiotensin II-infused CTLA-4-Tg/Apoe−/− mice had a markedly reduced number of CD4+Foxp3+ Tregs compared with angiotensin II-infused Apoe−/− mice. Here, AGT is linked to triple-A syndrome.