The role of smoking in the promotion of systemic inflammation and its potential link to the pathogenesis of the AF substrate has been partially elucidated, as smoking increases serum levels of Il-18 and -1β over two- to sevenfold [56] when compared to non-smokers, which marks excessive NLRP3 inflammasome activation. The gene discussed is NLRP3; the disease is atrial fibrillation.