While the elastase-CaCl2 model successfully reproduces phenomena such aortic dilation, elastin degradation, and inflammatory cell infiltration, it lacks features such as atherosclerosis and intraluminal fibrosis, which are commonly found in human AAA lesions and have a major impact in AAA progression (Golledge et al., 2006; Tanaka et al., 2009). Here, ELN is linked to triple-A syndrome.