This may occur as a consequence of an imbalance between CaV-dependent glutamate release and clearance of glutamate at cortical excitatory synapses, which might be created by enhanced CaV2.1-dependent glutamate release (as in FHM1) [23, 26, 41] or reduced clearance of glutamate by astrocytes (as in FHM2) [10, 27] or other mechanisms, which remain to be uncovered (as in common migraine with aura). This evidence concerns the gene ATP1A2 and migraine disorder.