We also assessed the impact of additional Rabs that have not been shown to be direct LRRK2 substrates but have been recently implicated in PD risk, Rab21 and Rab32 [66–68], and found that knockdown of both of these Rabs also significantly impaired endolysosomal GCase activity (Supplementary Fig. S6D and E). This evidence concerns the gene RAB32 and Parkinson disease.