Both clinical and preclinical evidence support these findings; overexpression of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, observed in CHIP patients [41], within cardiomyocytes has been shown to increase atrial fibrosis and susceptibility to AF, underscoring the role of inflammation-induced fibrotic remodeling in arrhythmogenesis [60,61,62]. Here, NLRP3 is linked to atrial fibrillation.