The fact that LRRK2 mutations are highly penetrant but progress very slowly312, while GBA1-PD mutations have low penetrance and progress rapidly316 supports the notion that these two subtypes of PD are likely to be driven by completely different underlying biochemistries, despite the fact that a large number of studies in cell culture and animal models purport to link GBA1-PD and LRRK2-PD. This evidence concerns the gene GBA1 and Parkinson disease.