There is no direct evidence that IS affects AF through activation of the NLRP3 inflammasome, but there is correlative evidence confirming the ability of IS to upregulate NLRP3 inflammasome components (NLRP3, ASC, and procaspase-1), which contributes to cardiomyocyte apoptosis and fibrosis. The gene discussed is NLRP3; the disease is atrial fibrillation.