It focused on GlcCer in non-GBA1-associated PD, but it would have been valuable to include some confirmed GBA1 mutant patients and GBA1-mutant mice for comparison as “positive” control, particularly because we did not find quantifiable glucosylsphingosine species in our lipidomic analysis, which are supposed to be biomarkers for Gaucher disease. This evidence concerns the gene GBA1 and Gaucher disease.