The angiotensin system and TGF‐β1 play an important role in atrial fibrosis‐associated with the heart failure models of AF,29, 30 a mouse model of AF30 and in human AF associated with heart failure.31 Ang‐II can stimulate NADPH oxidases 2 (Nox2) activity through the TGF‐β1 pathway and inhibition of TGF‐β1 blunts reactive oxygen species (ROS) formation.32, 33 Therefore, renin–angiotensin–aldosterone system (RAAS)–induced TGF‐β1 pathway and TGF‐β1–induced ROS may contribute to fibrotic remodelling. This evidence concerns the gene REN and atrial fibrillation.