Cardiac sodium channel (NaV1.5) loss of function is a critical mediator of cardiac conduction slowing, predisposing to ventricular arrhythmias and sudden cardiac death (SCD), both in acquired pathologies (ischemia, hypertrophy, heart failure) and inherited cardiac disorders caused by mutations in SCN5A, the gene encoding NaV1.5 [1, 2]. This evidence concerns the gene SCN5A and cardiac hypertrophy.