Previous research hasdemonstrated that TREM-1 can exacerbate experimental AAA by modulatingangiotensin II-induced monocyte trafficking and vascular wall inflammation [23].Although the specific ligands for TREM-1 have yet to be definitively identified,several studies have suggested that HMGB1 could be a potential TREM-1 ligandinvolved in the inflammatory response [24, 25]. This evidence concerns the gene HMGB1 and triple-A syndrome.