GBA1 mutations principally perturb lysosomal glucocerebrosidase activity, lysosomal clearance, and α-synuclein homeostasis; given paraxanthine’s reported promotion of autophagy and lysosomal competence in other models, it is biologically plausible that paraxanthine could attenuate GBA1-related vulnerability, but empirical data are sparse and warrant investigation in polygenic and genotype-specific PD models. Here, GBA1 is linked to Parkinson disease.