Given the involvement of ERK and DARPP-32 in LIDs, as indicated by studies performed in rodent models [5], [6], [7], these results are compatible with the hypothesis that coordinated activation of cAMP/PKA/DARPP-32 and ERK is implicated in the priming processes underlying the emergence of dyskinesia. The gene discussed is PPP1R1B; the disease is drug-induced dyskinesia.