Transgenic mice overexpressing human TorsinA[ΔE] under the immediate-early promoter from cytomegalovirus (CMV) did not develop dystonia, although a deficit in motor learning was identified [25], as well as a reduced response to amphetamine [28] and changes in the bidirectional plasticity of glutamatergic synapses between cortical neurons and striatal medium spiny neurons [29]. The gene discussed is TOR1A; the disease is Dystonia.