Based on our finding that VSMCs are the major origin of TLR4 expression in AAA, we would therefore evaluate whether TLR4 ligation by HMGB1 might enhance the proinflammatory response (e.g., cytokine release) in VSMCs in vitro and whether blockade of TLR4 signaling inhibits the action of HMGB1 on VSMCs. This evidence concerns the gene HMGB1 and triple-A syndrome.