Endothelial dysfunction is essential in the pathogenesis of AS (7–10), which releases inflammatory cytokines to VSMCs contributing to AS, including interleukin-1β (IL-1β), tumor necrosis factor-a (TNF-α), and transforming growth factor-β (TGF-β) (11, 12). This evidence concerns the gene TGFB1 and aortic stenosis.