Apart from the case of rare familial forms due to specific genetic mutations in the SNCA locus (i.e., increased protein expression due the gene dosage effect and tendency to form oligomers as a result of certain point mutations), the nature of mechanism(s) that promote α-syn aggregation in other forms of PD (genetic or idiopathic) remains elusive, and the mechanisms are likely to be of multi-factorial origin [1]. The gene discussed is SNCA; the disease is Parkinson disease.