Since both LRRK2 and GBA participate in the lysosomal-autophagy pathway involved in PD pathogenesis[51] and mutation carriers for both genes display the presence of Lewy bodies in the PD brain[52, 53], our results suggest that the LRRK2-GBA interaction may facilitate the autophagy-dependent impairment and the accumulation of α-Synuclein in dopaminergic neurons. Here, GBA1 is linked to Parkinson disease.