Using angiotensin-II (Ang-II) infusion-induced experimental AAAs in apolipoprotein E-deficient (Apoe−/−) mice, we tested whether IgE actions on T cells, MCs, and macrophages contribute to AAA pathogenesis and whether inhibition of IgE activity using FcεR1-deficient mice or ablation of plasma IgE using anti-IgE monoclonal antibody (mAb) ameliorates AAA development. This evidence concerns the gene APOE and triple-A syndrome.