Thus, it is possible that the degeneration and a minor loss of Purkinje cells together with the concurrent presence of neuroinflammation (Figure 2F–I), as well as the electrophysiological changes present in the Purkinje cells, as suggested by Duarri et al [15], may all contribute to the ataxia phenotype in mice carrying the Kcnd3 F227del mutation. This evidence concerns the gene KCND3 and cerebellar ataxia.