Based on the above data, the reductions in putative ERRγ targets in DAergic neurons from patients with Lewy body pathology12, and prior evidence for synuclein-induced mitochondrial impairment45,46, we sought to explore several possibilities: (1) whether deficiency in ERRγ could render DAergic neurons more vulnerable to synuclein-mediated toxicity, (2) if overexpression of ERRγ could be neuroprotective in models of synucleinopathy, and (3) whether deficiencies in ERRγ-dependent transcription could be caused by synucleinopathy. The gene discussed is SNCA; the disease is synucleinopathy.