However, there are several key barriers intrinsic to the existing models, including the inconsistent aneurysm incidence and suboptimal penetrance (particularly for systemically induced models), minimal rupture risks in abdominal aortas (e.g., unmodified elastase model and conventional AngII model), technical difficulties (e.g., intraluminal elastase perfusion model), etc. Indeed, no single experimental model described above fully recapitulate the pathophysiologies of AAA in patients. This evidence concerns the gene AGT and aneurysm.