MSA is a rapidly progressive synucleopathy arising from the misfolding and accumulation of SNCA species, mainly in oligodendrocytes [19], but transgenic models directing mutant SNCA to oligodendrocytes replicate only some aspects of human MSA [20,21], likely owing to complex genetics [22,23] and confounding lipid mediators such as glucosylceramides [24,25,26,27,28] and monounsaturated fatty acids [29,30,31] that can amplify the pathology of SNCA [32]. The gene discussed is SNCA; the disease is multiple system atrophy.