Our previous study using atherosclerotic CTLA-4-Tg/Apoe−/− mice revealed that CTLA-4 transgenic CD4+ T cells have a lower proliferative capacity than wild-type CD4+ T cells upon anti-CD3 antibody stimulation12, indicating the possible involvement of the cell intrinsic mechanism for CTLA-4-mediated protection from AAA as well as atherosclerosis. The gene discussed is CTLA4; the disease is triple-A syndrome.