Previous work also indicates that ectopic expression of human α-synuclein in Drosophila confers only mild phenotypic consequences [25, 45], so it is also possible that the influence of glucocerebrosidase deficiency on α-synuclein toxicity is not readily evident in Drosophila. While we fully acknowledge these potential confounds, several compelling observations suggest that a loss-of-function mechanism best explains the influence of GBA1 mutations on PD and DLB. Here, GBA1 is linked to Parkinson disease.