Moreover, migraine is one of the PRRT2‐related phenotypes,[26] even though PRRT2 variants are considered to be risk‐modifying rather than disease‐causing for migraine.[105] Altered functions of several interacting partners of PRRT2—such as the α3 isoform of Na+/K+‐ATPase (encoded by Atp1a3) and the CaV2.1 calcium channel (encoded by Cacna1a)—have been associated with changes in the susceptibility to spreading depolarization in various brain regions.[106, 107] As reviewed earlier (Section 2.2), these proteins are also associated with a variety of paroxysmal movement disorders. Here, ATP1A3 is linked to migraine disorder.