Given the broad heterogeneity in suspected mechanisms of both disease initiation and progression indicated by a variety of genetic and environmental factors, including neuroinflammation, genetic predisposition to energetic deficits, α-synuclein templating, and lysosomal function, it is not surprising that a one-size-fits-all approach for disease modification has failed in clinical trials for PD. This evidence concerns the gene SNCA and Parkinson disease.