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). The gene discussed is NLRP3; the disease is atrial fibrillation.