As early as 7 days of the AngII infusion, suprarenal aortas of COMP–/– mice released more MCP-1 and IL-6, exhibited greater MMP-9 activity and produced more reactive oxidative species (ROS) (Supplementary information, Fig. S2c–e), which have all been demonstrated to mediate AAA formation.34–36 Interestingly, even without AngII infusion, COMP deficiency alone markedly increased basal vascular wall inflammation, MMP activity, and oxidative stress, which may profoundly contribute to AngII-induced AAA formation (Supplementary information, Fig. S2b–e). This evidence concerns the gene CCL2 and triple-A syndrome.