A preclinical study suggested that sodium channel activity could help maintain VF.37 The Na+ accumulated in the cytosolic can drive Ca2+ entry through the Na+-Ca2+ exchanger, and causes cytosolic and mitochondrial Ca2+ overload and eventual decline in myocardial function.38,39 This may explain why amiodarone and lidocaine, which are sodium channels blockers, could improve the outcomes of shock-refractory VF/pVT. The gene discussed is SLC8A1; the disease is ventricular fibrillation.