Lysosomal acidification is critical for both chaperone-mediated autophagy (CMA via LAMP2A) and glucocerebrosidase activity (GCase/GBA1). The convergence hypothesis proposes that simultaneous dysfunction of both pathways creates a catastrophic failure of lysosomal proteostasis. This challenge seeks to establish: (1) whether the two deficits are truly synergistic (not merely additive), (2) the molecular mechanism linking them, and (3) whether restoring lysosomal pH via acidifying agents (or TFEB activation) can rescue both. Falsifiable prediction: dual knockdown of GBA1 and LAMP2A in dopaminergic neurons should increase SNCA aggregate burden by >2× versus single knockdowns combined, rescued by acidifying nanoparticles.