Sex is the largest nonmodiiable risk factor for the development of abdominal aortic aneurysms (AAAs) in humans and experimental models. Data from several studies consistently demonstrate a higher AAA prevalence in males than in females, contributing to divergent recommendations for AAA screening in men and women. Despite a higher AAA prevalence in males, females have more rapid rates of aneurysm dilation, and aneurysms rupture at smaller sizes. Unfortunately, no therapies have been efective to retard aneurysm dilation in either sex. Results from experimental AAA models indicate a protective role for estrogen in AAA development and progression, while male testosterone has been demonstrated to markedly promote angiotensin II (AngII)-induced AAAs. Potential mechanisms implicated in sex hormone regulation of AAAs include regulation of inlammation, matrix metalloproteinases, aromatase activity, oxidative stress, stem cells, and transforming growth factor-beta. In addition to sex hormones, sex chromosomes have been implicated in diseases of the aorta. Turner's syndrome (monosomy X) patients have a high incidence of thoracic aortic rupture. Recent studies indicate a novel approach to deine the relative role of sex hormones versus sex chromosomes in experimental AAAs. Further studies are warranted to determine interactions between sex hormones and sex chromosomes in AAA development and progression.