In SARS-CoV-2 infection, incriminated proarrhythmogenic mechanisms include impaired electrical conduction due to direct viral myocardial injury, release of cytokines predisposing to arrhythmogenicity (e.g., IL-6), pericardial effusion (sometimes associated with acute myocarditis), ischemia due to microthrombi in the coronary circulation and arrhythmogenic substrate due to post-myocarditis fibrosis or scar tissue [28,29]. The gene discussed is IL6; the disease is myocarditis.