CD14 and triple-A syndrome: IL‐6 is a key inflammatory cytokine in AAA formation.49 In the murine AngII infusion model, IL‐6 expression was highest in the adventitia and correlated anatomically with macrophage precursor recruitment.50–51 Also, expression of IL‐6 was markedly increased in human AAA compared with atherosclerotic, nonaneurysmal aorta.12,29 Further, we observed that CD14 expression was much higher in human AAA and colocalized with macrophages and that monocyte binding to AngII‐infused aorta was CD14 dependent.