Interestingly, AT1b receptor is associated with AngII-induced vascular contractility, but not with AngII-induced aortic pathologies.41 AngII-induced AAA formation primarily depends on AT1a receptor-mediated vascular oxidative stress, inflammation, and MMP activation or matrix degradation in mice.42 AT1a deletion or inhibition abolishes AngII-induced AAA formation in mice.43 Therefore, we speculated that COMP deficiency may increase vascular AngII levels, upregulate AT1a receptor expression, or induce AngII downstream signaling activation. The gene discussed is AGT; the disease is triple-A syndrome.