There are three classical forms of hereditary epilepsies associated with mutations of SCN8A, early infantile epileptic encephalopathy type 13 (EIEE 13), benign familial infantile seizures-5 and paroxysmal dyskinesia with SUDEP, which is the primary cause of epilepsy-related death from mutations of SCN8A. One possible explanation for the relationship between SCN8A-related epilepsy and SUDEP is the broad expression of NaV1.6 in ventricular myocytes and cardiac tissues [118, 119]. This evidence concerns the gene SCN8A and paroxysmal dyskinesia.