Although the initiating events are not fully elucidated yet, inflammation was shown to be a major contributing factor to AAA formation and progression.2 AAA formation is characterized by proinflammatory cell infiltration, including monocytes and macrophages, the release of cytokines and proteases and breakdown of extracellular matrix (ECM) proteins.2, , -5 Especially, the destruction of medial elastin and collagen (type I and III) causes an ongoing reduction of the stability of the aortic wall leading to an increasing inability to withstand the high intraluminal pressure.6,7. This evidence concerns the gene ELN and triple-A syndrome.