Increasing evidence has demonstrated that the Ang II cell membrane receptor, mainly angiotensin II type 1 receptor (AT1R), which via multiple signaling pathways, such as transforming growth factor-β (TGF-β)/mothers against decapentaplegic 2/3 (Smad2/3) and NACHT, LRR, and PYD domains-containing protein-3 (NLRP3)/nuclear factor kappa-B (NF-κB), regulate fibrosis formation and inflammation, and play a prominent role in AF (5). This evidence concerns the gene NLRP3 and atrial fibrillation.