In the present study, we found that hypertension stimulated CXCR2 activation, which activated several downstream signalling pathways, including NF‐κB, NADPH oxidase and TGF‐β1/Smad2/3, which promoted pro‐inflammatory, pro‐oxidative and pro‐fibrotic effects that led to AF. This evidence concerns the gene FMO5 and hypertensive disorder.