Ablation of D2 from CIN prevented this L-DOPA-associated increase in CIN phosphorylated rpS6<sup>240/244</sup>.<h4>Discussion</h4>Together, these findings indicate that D2 signaling in CIN promotes LID formation and suggest that CIN D2 is a potential molecular target for mitigating dyskinesias while preserving the therapeutic efficacy of L-DOPA. Here, RPS6 is linked to drug-induced dyskinesia.