Prior evidence has also shown that Itsn1 null mice exhibit PD-related phenotypes, including abnormal gait, limb grasping deficits, and decreased prepulse inhibition.33 Collectively, these data establish ITSN1 as a genetic cause of PD and suggest that it may interact with α-synuclein-mediated pathogenic mechanisms. The gene discussed is SNCA; the disease is Parkinson disease.