Here, we report that aneurysm formation in BMT ApoE−/− mice treated with Ang II was absent and required an increase in the dose of Ang II to achieve the same degree of aneurysm formation and rupture to that of non-BMT ApoE−/− mice treated with Ang II, highlighting the need to interpret BMT and Ang II-induced AAA studies more critically. The gene discussed is AGT; the disease is triple-A syndrome.