Knockout of the subtype Ucp-2 was reported to increase AAA incidence, promote elastin degradation and destruction of the aorta via upregulation of MMP2 and MMP9, increase oxidative stress, decrease SOD, and induce VSMC apoptosis in ApoE-/- AAA mice compared to Ucp+/+ aneurysm and wild type controls enzyme system. The gene discussed is UCP2; the disease is triple-A syndrome.