The results showed that colchicine treatment significantly reduced β-catenin accumulation in α-SMA-positive SMCs in AAA lesions from C57BL/6 and Apoe-/- mice (Fig. 4D and Fig. S9), and reduced GSK-3β phosphorylation and β-catenin nuclear translocation in AAA lesions from peri-aortic CaPO4-injured mice and in cultured human aortic SMCs in response to PDGF-BB stimulation (Fig. 4E-G). Here, APOE is linked to triple-A syndrome.