While UCP-2 has been found to increase endothelial nitric oxide synthase (eNOS) expression, inhibit apoptosis of cells from vessel walls and decrease ROS production [23], we measured the eNOS expression in aorta from different genotype mice and found it higher in WT mice than the UCP-2 KO mice before Ang-II infusion (S2 Fig) and lower in UCP-2-/-ApoE-/- mice than UCP-2+/+ApoE-/- mice after 4 weeks Ang-II treatment (Fig 5C), indicating that UCP-2 deficiency impaired the function of eNOS, and which could participates in formation of AAA. Here, APOE is linked to triple-A syndrome.