In addition, TGF-β/Smad signaling, which plays a key role in promoting tissue fibrosis, was also markedly activated in the lungs of G3 Terc−/− mice, indicating that shorting telomeres might enhance fibrosis via activation of TGF-β/Smads signaling, which is also the key pathway in cardiac fibrosis and AF persistency (33). This evidence concerns the gene TERC and atrial fibrillation.