Our previous study showed that c-Jun N-terminal kinase (JNK) inhibitor attenuated nicotine plus AngII-induced AAA formation by suppressing MMP-9, MMP2, monocyte chemotactic protein- (MCP-) 1, and regulated upon activation normal T cell expressed and secreted (RANTES) secretion from macrophages and VSMCs, suggesting that JNK was a signaling molecule in the pathogenesis of nicotine plus AngII-induced AAA [16]. This evidence concerns the gene CCL5 and triple-A syndrome.