The in vivo results showed that Ang‐(1–7) inhibited the incidence and progression of Ang II‐induced AAA by suppressing macrophage infiltration, inhibiting the expression of the inflammatory factors IL‐6, TNF‐α, CCL2 and the protease MMP‐2, and reducing the apoptosis of VSMCs. The gene discussed is CCL2; the disease is triple-A syndrome.