Taken together, the three different forms of FHM indicate the existence of a main pathophysiological pathway that, starting from excessive neuronal release of glutamate (CACNA1A), impaired glutamate reuptake by glial cells (ATP1A2), or enhanced glutamatergic activity due to impaired GABAergic inhibition (SCN1A), ultimately leads to altered glutamatergic neurotransmission, with consequent neuronal hyperexcitability and increased susceptibility to CSD (Ferrari et al., 2015). The gene discussed is SCN1A; the disease is familial hemiplegic migraine.