FGF-23 combined with FGFR4 produced ROS, activated downstream STAT3 and Smad3 proteins, and stimulated expression of matrix metalloprotein-2 (MMP-2) in myocardial tissue of patients with atrial fibrillation, leading to myocardial fibrosis (Dong et al., 2019). This evidence concerns the gene FGFR4 and atrial fibrillation.