D2 receptor-expressing cell-specific DYT1 conditional KO mice, used as a transgenic model of DYT1 early-onset generalized torsion dystonia, highlight locomotor deficits that are demonstrated in the accelerated rotarod and beam-walking tests and a significant reduction in striatal torsinA, acetylcholine metabolic enzymes, tropomyosin receptor kinase A (trk A), cholinergic interneurons, dimers of D2 receptors and tyrosine hydroxylase [65]. The gene discussed is TOR1A; the disease is Torsion dystonia.