Evidence of SNCA multiplications and constitutive phosphorylation in synucleinopathies suggests overexpression and toxic gain of function as a causative factor of disease, supported by increased neuronal cell death being associated with altered SNCA expression in patients with PD and in model systems (7, 8, 9, 10, 11, 12, 13). The gene discussed is SNCA; the disease is Parkinson disease.