Because GPNMB itself can modulate the microglial phenotype, promote phagocytic clearance, and influence α-synuclein processing, its genetic association, disease-specific upregulation, and biomarker profile in GD together point to its involvement in a shared lysosomal–neuroinflammatory axis that connects GBA1-linked metabolic defects with PD neurodegeneration. This evidence concerns the gene GPNMB and Parkinson disease.