Subsequently, the role of the AngII/AT1R signaling pathway in AAA-VSMCs has been gradually clarified, and the current research has found that the binding of Ang II to AT1R can active ERK/MAPK, PI3K/Akt, and JAK/STAT pathways, shifting VSMCs from a contractile to a synthetic phenotype [160,161,162]. The gene discussed is SOAT1; the disease is triple-A syndrome.