Although the ability of nicotine to induce the development of AAA in ApoE−/− mice model has been proved [4, 5] and AngII alone was able to induce the AAA formation in ApoE−/− mice [17, 18], a more physiologically relevant experimental model without the interference of lipid metabolism is necessary and the underlying mechanisms remain to be studied. This evidence concerns the gene APOE and triple-A syndrome.