A previous study suggests that IL-17 is a critical mediator of elastase-induced AAA and genetic deletion of IL-17 not only protects mice against AAA formation but also leads to significant reduction of several inflammatory cytokines (TNF-α, IFN-γ and MCP-1), indicating that IL-17 is an upstream mediator of the inflammatory cascade23. This evidence concerns the gene IL17A and triple-A syndrome.