Disruption of FGF14 in the fgf14−/− experimental model also leads to paroxysmal dyskinesia and ataxic gait attributed to dysfunction of GABA signalling in the basal ganglia that are remarkably similar to the motor features of SCA27 and paroxysmal hyperkinesias in some FGF14 mutations [20]. Here, FGF14 is linked to spinocerebellar ataxia type 27.