Scn10a−/− mice exhibit shorter PR intervals11 and a gain-of-function single nucleotide polymorphism in SCN10A that prolonged PR interval was strongly associated with a decreased risk of ventricular fibrillation in the setting of acute myocardial infarction11, suggesting a beneficial role for higher SCN10A expression in cardiac electrophysiology. Here, SCN10A is linked to ventricular fibrillation.