recently discovered that in angiotensin II‐induced AAA, the transfer of Tregs reduced vascular inflammation and delayed the process of AAA;[6] otherwise, removing Tregs increased tissue inflammation and aggravated AAA.[7] These studies suggest that Tregs are involved in the regulation of chronic inflammation in AAA and are likely to be a potential target for treatment of AAA. The gene discussed is AGT; the disease is triple-A syndrome.