Increased Nlrp3 inflammasome activation in cardiomyocytes is known to promote aberrant SR calcium release, promote electrical remodeling leading to shortening of atrial APD, and increase susceptibility for AF in mouse models.8,9,30 It is evident that further investigation is required to determine the molecular mechanisms that connect Nlrp3 activation, CaMKII, and SR calcium release, and how loss of Tet2 in macrophages contributes to these alterations. The gene discussed is NLRP3; the disease is atrial fibrillation.