While also present in individuals with GABRB3 GOF, the high prevalence of movement disorders generally considered to depend on basal ganglia dysfunction (i.e., dystonia, chorea, dyskinesia and athetosis) is striking in individuals with GABRB2. This could suggest that β2-containing receptors play a relatively greater role in the disinhibitory circuits in the basal ganglia that initiate movement. This evidence concerns the gene GABRB2 and drug-induced dyskinesia.