Using Ang-II infusion-induced experimental AAAs in Apoe−/− mice, FcεR1-deficient mice, adoptive transfer of leukocyte populations, and anti-IgE mAb administration, we demonstrated that IgE actions on CD4+ T cells, MCs, and macrophages, and possibly other inflammatory and vascular cells contribute to AAA pathogenesis. The gene discussed is CD4; the disease is triple-A syndrome.