The pathogenesis of AAA is closely linked to the degradation of the ECM, a process critically mediated by (MMPs, particularly MMP2 and MMP9.[31] MMP2, primarily secreted by fibroblasts and SMCs, is responsible for the degradation of collagen and elastin, while MMP9, mainly produced by macrophages, drives inflammatory ECM remodeling.[32] Despite their essential roles in ECM breakdown, clinical trials targeting these MMPs have consistently failed to yield effective therapies for AAA,[33] suggesting that inhibition of MMP activity alone does not sufficiently address the complex pathology of AAA. This evidence concerns the gene ELN and triple-A syndrome.