We critically compare commonly used abdominal aortic aneurysm (AAA) models (angiotensin II ± hyperlipidemia, elastase, calcium chloride, β-aminopropionitrile BAPN hybrids, and mineralocorticoid agonist/fludrocortisone models) with thoracic aortopathy and dissection models (BAPN alone or with AngII, genetic models including Marfan and smooth muscle contractile mutations, and AngII + TGF-β blockade). The gene discussed is AGT; the disease is hyperlipidemia.