The mutations in SCN1A result in a wide range of epilepsies that differ in their comorbidities and functional deficits, such as Dravet syndrome (DS), genetic epilepsy with febrile seizures plus (GEFS+), and developmental and epileptic encephalopathies (DEEs), which further comprises myoclonic-atonic epilepsy (MAE) and epilepsy of infancy with migrating focal seizures (EIMFS) [198,199]. This evidence concerns the gene SCN1A and epilepsy with myoclonic atonic seizures.