Studies using cells transfected with mutant ATP1A3 have suggested mutations may reduce affinity for Na+ and that the resultant dysfunction in ion transport may impair cell viability, but the relative importance of these mechanisms to the actual pathophysiology of rapid onset dystonia-parkinsonism remains uncertain (Rodacker et al., 2006; Blanco-Arias et al., 2009). This evidence concerns the gene ATP1A3 and Dystonia.