Variants of the SCN5A gene that encodes α-subunit of the cardiac sodium channel (Nav1.5) cause various genetic arrhythmias known as ‘sodium channelopathy’1 Particularly, SCN5A loss of function (LOF) are associated with arrhythmia disease including Brugada syndrome (BrS), idiopathic ventricular fibrillation, cardiac conduction defects, supraventricular tachycardia (SVT), or dilated cardiomyopathy.2 This evidence concerns the gene SCN5A and paroxysmal familial ventricular fibrillation.