Although our findings will need to be confirmed in a synucleinopathy model that expresses wild-type human α-syn [28], our results using M83 transgenic mice suggest that PrPC may not be an ideal therapeutic target for blocking the cell-to-cell propagation of α-syn aggregates in synucleinopathies such as PD and MSA. The gene discussed is PRNP; the disease is synucleinopathy.