stenosis. 11 Among them, inflammatory cells and cytokines play an important role in AAA occurrence and expansion. 12-14 Consistently, inhibition of tumor necrosis factor (TNF)-α, the complement system and peroxisome proliferator-activated receptor γ successfully prevented AAA formation and expansion in mouse AAA models. 15 In contrast, anti-transforming growth factor-β (anti-TGF-β) antibody injection induced AAA rupture in an angiotensin II-stimulated AAA model, 16 indicating that upregulated TGF-β plays a protective role against AAA progression and rupture. 16,17 Taken together, at least in animal models, the mechanism underlying AAA expansion is not similar to that underlying the occurrence of AAA. Risk Factors for AAA Occurrence, Expansion, and Rupture in Humans Consistent with the aforedescribed experimental findings, the risk profiles of occurrence, expansion, and rupture of AAA are different from one another in humans. Except for AAA caused by infection, trauma, or Marfan syndrome, AAA occurrence is more prevalent in aged patients, male subjects, smokers, and those who have chronic obstructive pulmonary disease, hypertension, and low high-density lipoprotein cholesterol. 18 Many cohort studies identified smoking as the strongest risk factor for AAA formation. 19 A cohort study in Sweden suggested that