Two doses of anti-IgE antibody to Ang-II-infused Apoe−/− mice effectively ablated plasma IgE and inhibited AAA growth and associated lesion inflammation, apoptosis, microvascularization, and cell proliferation to the same extents as in Ang-II-infused Apoe−/−Fcer1a−/− mice. The gene discussed is AGT; the disease is triple-A syndrome.