Mechanistic insights have further refined our understanding of how SCN5A variants influence phenotype expression: Using combined genetic and high-density epicardial mapping, Ciconte et al. (43) demonstrated that SCN5A variant carriers exhibit a larger epicardial arrhythmogenic substrate, prolonged electrograms, and higher prevalence of spontaneous type I ECG and VT/VF events than non-carriers. Here, SCN5A is linked to ventricular fibrillation.