The characteristics and localization of the D1R-D3R heterodimer in the striatum suggest that this complex could be the functional unit mediating the development of levodopa (L-DOPA)-induced dyskinesia in PD models [52,57,58,59,60], thus providing a unifying mechanism for D1R- [52,61,62] and D3R-mediated alterations in the development of these side effects of L-DOPA therapy. This evidence concerns the gene DRD1 and Dyskinesia.