Given that our analysis of SCA1 and SCA2 models reveals dysregulation of not just Kcnma1, but also the ataxia-linked Ca2+ channel genes Cacna1g and Trpc3, we chose to focus on these three channels and to expore the hypothesis that severe Purkinje neuron dysfunction observed in SCA1 might arise due to synergistic dysfunction of an ion channel module that contains BK and these Ca2+ sources (Fig. 2C). This evidence concerns the gene ATXN2 and cerebellar ataxia.