Recent studies demonstrate that cardiomyocyte (CM) NLRP3 (NACHT, LRR, and PYD domains-containing protein-3) inflammasome activation and NF-κB activation are key proarrhythmic mediators of multiple pathophysiological signals in AF and have direct effects on atrial fibrosis, ion channel, and connexin dysfunction in mouse and rabbit atria (4, 6, 7). Here, NFKB1 is linked to atrial fibrillation.