Indeed, neuronal ubiquitinopathy preceding an increase in alpha-synuclein levels has been described in a GBA1 knock-in mouse model (33) and it is likely that gba1−/− zebrafish represent an example of non-synuclein proteinopathy and synuclein-independent neurodegeneration occurring in the absence of GCase activity. This evidence concerns the gene SNCG and alpha synuclein measurement.