Although the genetic linkage of GBA1 mutations and PD in humans is clear, the lack of nigrostriatal degeneration in these two models could provide evidence for either unique biology within the mouse that intervenes and masks the role of decreased GCase activity in exacerbating PD-related pathology, and/or a mutation-dependent toxic gain-of-function effect of various GBA1 mutations in driving pathology. Here, GBA1 is linked to Parkinson disease.