Synuclein is the obvious primary target, and options include including passive immunotherapy, active immunotherapy, aggregation inhibitors, antisense oligonucleotides, etc. Lysosomal dysfunction also seems to be a critical in iRBD pathophysiology, and agents targeting glucocerebrosidase A-related mechanisms are currently in trials in PD (e.g. GCAse activators and chaperones). This evidence concerns the gene SNCA and Parkinson disease.