These data suggest that changes in the pattern of oscillatory activity, rather than modifications in the firing rate alone, are involved in PD dyskinesia (Obeso et al., 2000), but decreased GPi firing rates cannot completely explain LID because lesions of GPi or stimulation both silence these neurons and lead to LID abolition (Obeso et al., 2000). The gene discussed is GPI; the disease is drug-induced dyskinesia.