This can be explained by activation of KCa2.1 and KCa2.2 channels with a more widespread expression in the murine brain [22] and is in line with findings that higher doses of SKA-31 are anticonvulsant presumably due to KCa2.2 activation [30] and acutely improve motor deficits in SCA3 mice, a model of spinocerebellar ataxia 3 [44]. This evidence concerns the gene KCNN2 and Machado-Joseph disease.