In fact, endogenous antioxidantdefenses [such as Cu/Zn and Mn superoxide dismutase, glutathione reductaseand glutathione peroxidase,−,  Paraoxonase-1, Nrf2/Heme-oxygenase 1 andGlutathione-SH] were shown to be dysregulatedin AAA and PAD, as described in a recent review. Moreover, our results agree with the ones previously reportedfor atherosclerotic AAA and thoracic AAA (atherosclerotic and nonatherosclerotic),where the authors found reduced levels of PE plasmalogens in aortictissue samples. The gene discussed is HMOX1; the disease is triple-A syndrome.