Immunofluorescent staining showed that SOST silencing reduced AAA lesion SMC contractile phenotype (TAGLN+α-SMA+) and endothelial KLF4 expression, increased synthetic SMC contents (KLF4+α-SMA+, CD68+α-SMA+) (Fig. 5G-I and Fig. S2F), and enhanced the β-catenin accumulation in α-actin-positive SMCs (β-catenin+α-SMA+) and VCAM-1 expression in ECs (Fig. 5J and Fig. S2E). This evidence concerns the gene SOST and triple-A syndrome.