However, in other studies, Prdx2 was found to be an inducer of ruptured AAA (Urbonavicius et al., 2009), while Prdx6 expression was elevated in patients with AAA; in addition, in AAA tissue, prdx6 colocalized with neutrophils, vascular SMCs, and oxidized lipids. This evidence concerns the gene PRDX6 and triple-A syndrome.