Our findings of significant downregulation of Sost accompanied by upregulated Spp1 and Mmp9 are in line with the study by Krishna et al. which demonstrated the potential of sclerostin in inhibiting dissecting AAA formation and atherosclerosis and provided evidence for epigenetic silencing of sclerostin in human AAAs.61 This evidence concerns the gene SOST and achalasia-alacrima syndrome.