No clustering between the different samples was detected (Fig. 2b, Supplementary Fig. 5) which is not surprising since 42 of the 63 samples come from PD patients (with and without GBA1 mutations); the fact that control samples did not cluster can likely be explained by the high variability in human brain samples between individual patients and the relatively small number of changes in protein levels (see below). This evidence concerns the gene GBA1 and Parkinson disease.