To further confirm our hypothesis, we use LY363947 (10 μM) [25], a TGFβR1 kinase activity inhibitor, to treat BMSCs with bleomycin and found that it markedly inhibited AF cell migration in both the scratch-wound healing and the transwell migration assay (Fig. 2a, b), and it could also mitigate the upregulation of these pro-fibrotic marker genes and proteins mentioned above (Fig. 2e, f). Here, TGFBR1 is linked to atrial fibrillation.