To elucidate the mechanisms of AAA formation, several animal models [i.e., chronic infusion of angiotensin II (AngII), local elastase infusion, and adventitial exposure of calcium chloride] are widely employed (Daugherty and Cassis, 1999; Chiou et al., 2001; Trachet et al., 2015) which exhibit features similar to human AAAs, including inflammatory cell infiltration, VSMC apoptosis and elastin fragmentation. Here, AGT is linked to triple-A syndrome.