However, eosinophilgene knockout exacerbated AAA growth with increased inflammatory infiltration andangiogenesis in Ang II-induced Apoe-⁣/- mice [61].Mechanistically, eosinophil-derived mouse eosinophil-associated-ribonuclease-1and interleukin (IL)-4 trigger the polarization of macrophages from M1 to M2,resulting in ECM remodeling and wall weakening [61]. The gene discussed is AGT; the disease is triple-A syndrome.