Using hypercholesterolemic DEREG mice, we demonstrated that genetic depletion of CD4+Foxp3+ Tregs aggravates AAA formation and rupture in angiotensin II-infused Apoe−/− mice by upregulating immunoinflammatory responses in the aneurysmal lesions, providing direct evidence for a protective role of CD4+Foxp3+ Tregs in the development of AAA [71]. The gene discussed is APOE; the disease is triple-A syndrome.