As far as cerebellar ataxia is concerned, the aforementioned observations support the idea that functional homeostasis of KV4.3 plays an imperative role in the operation of cerebellar physiology, and that both loss- and gain-of-function phenotypes of KV4.3 variant channels may considerably perturb neuronal excitability in the cerebellar circuit and therefore contribute to the pathogenesis of ataxia. Here, KCND3 is linked to aceruloplasminemia.