Supporting this concept, reduction of intracellular neuromelanin levels in vivo, either by boosting neuromelanin cytosolic clearance with the autophagy activator TFEB34 or by reducing neuromelanin production with VMAT2-mediated enhancement of dopamine vesicular encapsulation,80 resulted in a major attenuation of the PD phenotype, both at the behavioural and neuropathological levels, in AAV-hTyr-injected neuromelanin-producing rats. The gene discussed is SLC18A2; the disease is Parkinson disease.