The role of KCa3.1 in dystonia is poorly examined, however, genetic KCa3.1 deficiency was shown to lead to locomotor hyperactivity in mice [19] and the activator of KCa3.1, riluzole, was proposed as a therapy in an open-label pilot study and was also demonstrated to be beneficial in other movement disorders [20–24]. The gene discussed is KCNN4; the disease is Dystonia.