These results indicate that the abnormal accumulation of alpha-synuclein in DAns, a PD-relevant in vitro phenotype previously shown to be caused by impaired proteostasis24, is fully penetrant with the LRRK2 G2019S mutation and, therefore, does not appear to be modified by the genetic background of control, L2-PD or L2-NMC individuals. Here, LRRK2 is linked to Parkinson disease.