Despite the fact that knockout of the BK channel pore-forming subunit causes a profound ataxia (Meredith et al., 2004; Sausbier et al., 2004), the role of the β4 accessory subunit in the cerebellum is either more subtle or somewhat different since an ataxic phenotype has not been reported in β4 knockout mice. This evidence concerns the gene KCNMA1 and cerebellar ataxia.