These findings were confirmed by a recent paper from our laboratory that showed mice with low VMAT2 expression display increased formation of toxic dopamine metabolites, increased oxidative damage in dopamine-rich areas, and a Parkinson's disease-like phenotype [54], again supporting the idea that increased VMAT2 could be beneficial in the treatment of Parkinson's disease. The gene discussed is SLC18A2; the disease is Parkinson disease.