To further elucidate how DFO treatment could augment AAA severity, we tested HIF-1α expression in the whole aorta lysate and found that compared with the AngII-treated group, DFO treated mice had significantly higher HIF-1α expression in the aorta lysate and significantly increased MMP-2 and MMP-9 activities (n = 5, Supplementary Figure 3). The gene discussed is HIF1A; the disease is triple-A syndrome.