Genes with higher expression in AS included convergent pathways of fibrosis—many studied in pro-fibrotic mechanisms in other settings—including TGF-beta and extracellular matrix metabolism and fibroblast proliferation (WNT9A (fibroblast)44, ITGA6 (fibroblast, endothelial)45, AGRN (fibroblast, endothelial)46, CRIM1 (cardiomyocyte, fibroblast)47), promotion of epithelial-mesenchymal transition (SEMA4C (endothelial, fibroblast)48, LAYN (endothelial, fibroblast)42), pro-inflammatory phospholipid signaling (ENPP2/ATX49), and TNF-mediated inflammation, among others. This evidence concerns the gene SEMA4C and aortic stenosis.