Ever since α-synuclein (αS) was identified to be a primary component of Lewy bodies and Lewy neurites (1) in synucleinopathies, such as Parkinson’s disease (PD), dementia with Lewy Bodies (DLB) and multiple-system atrophy (MSA), the endeavors of many laboratories have coalesced around elucidating αS native structure, physiological function, aggregation propensity and cell toxicity. The gene discussed is SNCG; the disease is synucleinopathy.