The complexity of the interplay between protein and lipid homeostasis is also illustrated by the emerging relationship between lysosomal storage disorders and Parkinson’s disease, at least in part through the consequences of reduced glucocerebrosidase activity in lysosomes (Mazzulli et al., 2011), where one may expect the low pH to promote the proliferation of α-synuclein aggregates by secondary nucleation (Buell et al., 2014), which could follow the glycosphingolipid-dependent formation of initial α-synuclein seeds (Mazzulli et al., 2011; Zunke et al., 2018). This evidence concerns the gene GBA1 and Parkinson disease.