The transcription factor nuclear factor‐kappa B (NF‐κB), via alterations in angiotensin and redox signaling, enhances heterogeneity in conduction, thereby promoting intra‐atrial reentry.31, 32 Diabetic hyperglycemia leads to overproduction of ROS, leading to NF‐κB upregulation, in turn promoting the transcription of proinflammatory genes.33, 34 Together, NF‐κB‐mediated vascular inflammation, oxidative stress, vascular and myocardial dysfunction in diabetes mellitus play a pivotal role in the genesis of AF. This evidence concerns the gene NFKB1 and diabetes mellitus.