In addition to the difference in model organism used, the discrepancy of findings may be in part related to the different pathogenicity of VPS35 knock-down and D620N point mutation as D620N has been reported to result in a gain of function, causing PD through hyperactivation of the LRRK2 kinase [32] and alteration of the dopaminergic system [33]. The gene discussed is VPS35; the disease is Parkinson disease.