This EAG1 mutation with gain-of-function compared to that in other K+ channels with loss-of-function indicates that the mechanisms mediating the epilepsy may be different from that in classical types of epilepsy [109], although some sodium channel blockers and GABA receptor agonists such as rufinamide, topiramate, and nitrazepam have been used to control seizures on the KCNH1 mutation-affected cases [22]. The gene discussed is KCNH1; the disease is epilepsy.