GBA1 and Parkinson disease: Indeed, restoring enzyme activity by exogenous supply of a recombinant active GCase (i.e., enzyme replacement therapy) to the patient corrects most of the non-neurological symptoms (whether the parkinsonism associated with GD or heterozygosity for GBA1 mutations is solely due to reduced GCase activity or, alternatively, implicates a misfolded GCase protein prone to aggregation, is still a matter of debate).