The aggregation of α-synuclein is a key pathological hallmark in Lewy body diseases, including Parkinson's disease and dementia with Lewy bodies (DLB).1-4 α-Synuclein is thought to aggregate from its native intrinsically disordered monomeric form, undergoing a profound structural transition through an α-helical structure to a β-sheet-rich filamentous configuration.5,6 This process leads to the formation of toxic oligomers and protofibrils and fibrils, which ultimately mature to form neuronal cytoplasmic inclusions termed ‘Lewy bodies’.7 The gene discussed is SNCA; the disease is Parkinson disease.