Genetic deletion of Fgf14 in Fgf14−/− mice leads to severe ataxia, paroxysmal dystonia, and cognitive impairment (Wang et al., 2002; Wozniak et al., 2007) associated with deficits in synaptic plasticity in the hippocampus (Xiao et al., 2007) and neuronal excitability in the cerebellum (Goldfarb et al., 2007; Shakkottai et al., 2009). Here, FGF14 is linked to cerebellar ataxia.