Clusterin, MMP-7, junctional adhesion molecule A (JAM-A), cathepsin S, angiotensin-converting enzyme 2 (ACE-2), C–C motif chemokine 5 (RANTES), and oncostatin-M (OSM) have previously been reported to be associated with AAA development, reflecting the pathophysiological changes in AAA. This evidence concerns the gene ACE2 and triple-A syndrome.