TGF-β1 has been shown to be associated with the occurrence and progression of AF through a well-known pro-fibrotic mechanism47, and a recent study has shown that miR-181b mediates TGF-β-induced endothelial-mesenchymal transition involved in AF by targeting semaphorin 3A48. The gene discussed is TGFB1; the disease is atrial fibrillation.