Extensive clinical and basic studies have shown that Tregs play a protectiverole in the formation of AAA by regulating endogenous immune responses [46, 47, 48].In vitro studies have shown that Tregs can reduce the expression ofcyclooxygenase 2 and prostaglandin E2 in macrophages and VSMCs, increase VSMCactivity and induce macrophage differentiation from M1 to M2, thus reducing theoccurrence of AAA in Ang II-induced models [49, 50]. This evidence concerns the gene AGT and triple-A syndrome.