Moreover, compared to patients with lower risk of aneurysm rupture, the expression of AIM2 inflammasome core components (e.g., ASC, caspase-1, caspase-5) and its downstream product IL-1β were all conspicuously up-regulated in the peripheral blood single infiltrating lymphocytes of patients at higher risk, suggesting a correlation between AIM2 inflammasome and AAA rupture as well as indicating that AAA-associated lymphocytes could carry out AIM2 inflammasome signaling [58]. This evidence concerns the gene IL1B and triple-A syndrome.