Dysregulated lipid metabolism, particularly involving sphingomyelin and phosphatidylcholine, is thought to contribute to neurotoxicity by promoting the production of ceramide,15,16 which induces apoptosis through increased reactive oxygen species.17,18 Analysis of post-mortem Lewy bodies from Parkinson's disease cases has shown heightened glucocerebrosidase activity and lipid accumulation,19,20 including the presence of sphingomyelin and phosphatidylcholine20 and phosphoinositide,21 likely resulting from membrane disruption caused by pathological α-synuclein. The gene discussed is SNCA; the disease is Parkinson disease.