When comparing human AAA samples to healthy aortae, although protein expression of TIMP-2 was decreased while TIMP-1 and TIMP-3 were increased, heightened activity of MMP-1, MMP-9, MMP-12, and MMP-14 were observed (147), and therefore credited with the excess degradation of collagen and elastin, and driving aneurysmal dilatation. This evidence concerns the gene MMP1 and triple-A syndrome.