Whilst epilepsy mutations in the gene are usually loss-of-function and lead to reduced inhibitory interneuron firing, increased selective cortical interneuron firing, and therefore seizures [110], in FHM3, the gene mutations in migraine tend to cause gain-of-function and cause increased GABAergic firing, increased extracellular potassium and glutamate, and an increased propensity to CSD [111]. The gene discussed is SCN1A; the disease is migraine disorder.