Interestingly, eotaxin is elevated in the plasma of angiotensin II-infused HO-1−/−apoE−/− mice at 4 but not 2 or 3 weeks, suggesting lack of HO-1 increases eotaxin production at a later stage of AAA development, although the mechanisms by which HO-1 controls eotaxin expression remain to be determined. This evidence concerns the gene CCL11 and triple-A syndrome.