This shift has allowed new insights into a number of aspects of GD molecular and cellular pathology, including, as described throughout this review, electrophysiology, calcium signaling, inflammatory response, autophagic flux, lysosomal defects and, importantly, α-synuclein accumulation and the mechanistic relationship between GD and the Parkinson’s related synucleinopathies. This evidence concerns the gene SNCA and Parkinsonism.