We and others demonstrated previously that signaling pathways, such as c-jun N-terminal kinase (JNK) and nuclear factor (NF)-κB, play a key role in regulating the expression of proinflammatory mediators, including cytokines, and in activating MMPs in AAA and that inhibiting these signals is highly effective in treating experimental AAA [7,8,9]. This evidence concerns the gene NFKB1 and triple-A syndrome.