Most importantly, since the molecular mechanisms of the activations of TGF-β1/Smads, NLRP3 inflammasome, CTGF and Rac-1, and connexins remodeling all links to an increased angiotensin II, we can propose that a potential anti-AF approach for targeting the atrial structural remodeling by using angiotensin II antagonists is available to prevent AF in patients with CKD. This evidence concerns the gene TGFB1 and atrial fibrillation.