Finally, the identification of mutations in ANO3, which encodes a Ca2+-gated chloride channel predominantly expressed in the striatum, as a cause of craniocervical dystonia suggests that altered neuronal excitability due to ion channel pathology could also result in dystonia and raises the possibility that medication aimed at correcting the kinetics of the channel might be an effective treatment in a subset of patients. This evidence concerns the gene ANO3 and Dystonia.