Whilst CACNA1A mutations in migraine exhibit gain-of-function effects, ATP1A2 mutations produce loss-of-function of sodium–potassium ATPases and, in turn, rising K+ levels within the synaptic cleft, thus altering cell membrane sodium gradients in key astrocytic cells and affecting glutamatergic neurotransmission, as well as reducing extracellular potassium clearance [55]. Here, ATP1A2 is linked to migraine disorder.