CACNA1B and Familial paroxysmal ataxia: Cacna1b null mice exhibit a hyperkinetic movement disorder (37) and mutations in the homologous region of CACNA1A (Cav2.1), the subunit that together with Cav2.2 controls depolarization-induced calcium entry and transmitter release, were already reported to cause episodic ataxia and/or familial hemiplegic migraine (38).