In the inflammatory background of AAA and specifically in the cyto-chemokines-related pathways, the CXCR2/CXCL1/IL-8 axis represents a putative therapeutic target in AAA, playing a causal role and pharmacologically modulable on in vivo murine elastase-induced AAA [6] and in ex-vivo cultured AAA tissues, as recently proposed by our group [7]. The gene discussed is CXCR2; the disease is triple-A syndrome.