Dear Editor,rnGaucher disease (GD) is the most common lysosomal storage disease (LSD) caused by an insufficiency of the lysosomal enzyme glucocerebrosidase (GCase)[1].GCase insufficiency produces the excessive lysosomal accumula-tion of unmetabolized glycolipid substrates including glucosylceramide (GlcCer),leading to the disruption of the structure and function of tissues and organs,including the blood system,viscera,brain,bones,and cartilage.GD was initially classified into 1-3 types based on the variation of severity and progression in neuropathic manifestation,which is early onset,most severe and acute in type 2,later onset and chronic in type 3,and not obvious in type 1.However,accumulating evidence has shown that type 1GD is clearly associated with Parkinson\'s disease and related synucleinopathies [1].Currently,there are multiple available ways of treating GD patients,including enzyme replacement therapy,substrate reduction therapy,and pharmacological chaperone therapy [2].However,the therapeutic effect of these approaches used either alone or in combination in GD patients is unsatisfactory.New drug candidates have been studied for a long time in order to develop promising therapeutic approaches to benefit GD patients,especially those with pathological features in the central nervous system.