Thirdly, our observational findings are in line with experimental evidence linking matrix metalloproteinases to the onset and progression of AAA (Hellenthal et al, 2009), with MMP12 being highly expressed at disease sites and suggested to contribute to the degradation of elastic fibres and hence weakening and dilation of the aortic wall (Curci et al, 1998). The gene discussed is MMP12; the disease is triple-A syndrome.