GBA1 knockout mice and transgenic mouse lines carrying GBA1 point mutations well recapitulate GD phenotype, with accumulation of α-synuclein and ubiquitinated proteins, the presence of typical “Gaucher cells” and inflammation (28), but they also prove to be appropriate for the study of the effects of GCase reduction in PD pathogenesis. This evidence concerns the gene GBA1 and Parkinson disease.