Since PARKIN mutations account for about three-quarters of PD cases with an age at onset of 30 years or younger, understanding the pathophysiological mechanisms that underlie early and atypical dystonia and dyskinesia in PARKIN patients is a key step toward achieving a more personalized treatment for this genetic condition and toward understanding the biological basis of this phenomena in other early-onset genetic forms of PD. The gene discussed is PRKN; the disease is drug-induced dyskinesia.