Metabolic modelling further highlighted shared pressure points, including inositol phosphate signalling, glycerophospholipid turnover, glycolysis/gluconeogenesis, and catecholamine handling, while revealing subtype-specific weighting, with greater involvement of fatty acid and bile acid metabolism under GBA1 deficiency and additional perturbations in nucleotide, one-carbon, and sterol metabolism in sporadic PD. This evidence concerns the gene GBA1 and Parkinson disease.