Abstract Background Pathogenic SCN5A variants are associated with inherited arrhythmias such as long QT syndrome, Brugada syndrome, and sick sinus syndrome (SSS). While Na v 1.5, an α-subunit of the cardiac sodium channel encoded by SCN5A , has been considered to function as a monomer, recent studies reveal that a reduction of sodium current in wild-type (WT) Na v 1.5 can be caused by dimerization with loss-of-function (LOF) mutated Na v 1.5 through dominant-negative (DN) effects. However, the clinical significanc…