We have known that the tissue renin‐angiotensin system (RAS) hyperactivity and high expression are involved in the pathomechanism of cardiac fibrosis42; moreover, Ang‐II has also been reported to participate in the maintenance of AF by inducing atrial structural remodelling, which is characterized by interstitial fibrosis.43, 44. This evidence concerns the gene REN and atrial fibrillation.