TUBB4a is supposed to be involved in neuronal cytoskeletal defects (Hersheson et al., 2012), while ANO3 and GNAL mutations point to a key role for striatal neurons in the pathophysiology of dystonia, either through abnormal neuronal excitability related to the malfunctioning of chloride channels or through abnormalities of dopamine and/or adenosine signal transduction pathways (Charlesworth et al., 2012; Fuchs et al., 2013). This evidence concerns the gene ANO3 and Dystonia.