The sensitivity of SCV relationships dictating the NPC1 fold in disease to HDAC is generalizable given that HDACi correct a broad range of misfolding disorders that are triggered by genetic variation in the population, including cystic fibrosis38, alpha-1-antitypsin deficiency39,40,47, Gaucher’s disease65, and neurodegenerative aggregation-driven diseases including Friederich Ataxis66, Alzheimer’s, Parkinson’s, and Huntington67,68. This evidence concerns the gene HDAC9 and Parkinsonism.