The main findings of this study included: (1) Cav-1 was significantly downregulated at both transcript and protein levels, which was accompanied by an upregulation of TGF-β1, an increase of collagens content, and stimulation of atrial fibrosis in atrial tissues from AF patients relative to SR subjects; (2) Application of TGF-β1 to HAFs decreased the protein level of Cav-1; (3) Downregulation of Cav-1 in HAFs increased the TGF-β1-induced activation of Smad signal pathway and collagens production. This evidence concerns the gene TGFB1 and atrial fibrillation.