A therapeutic intervention dampening DA release from the serotonergic terminals might be effective in reducing dyskinesia, however in order to achieve substantial functional restoration in these cases, it would be necessary to provide an additional pool of DA that can normalize the activation pattern of DA receptors (increase occupancy at D2R and reduce activation of extrasynaptic D1R) and sustain this activity over a long term, e.g., by enriching the dopaminergic terminal density in denervated regions of striatum especially in areas that receive 5HT innervation. The gene discussed is DRD1; the disease is drug-induced dyskinesia.