Concerning animal models of AAA, the predominant model employed was Angiotensin II-induced AAA in mice, utilized in 18 studies followed by Elastase-induced (6 studies) [7, 16, 17], CaCl2-induced (5 studies), porcine pancreatic elastase (PPE)-induced (3 studies), hypoperfusion-induced (2 studies), nicotine-induced (1 study), and anti- Transforming growth factor-β (TGF-β)-induced (1 study). This evidence concerns the gene AGT and triple-A syndrome.