Furthermore, MPTP studies have shown that mitochondrial complex I inhibition in DA SNc neurons can result in a clinical phenotype that resembles that of idiopathic PD; the inhibition of complex I by paraquat and rotenone or the genetic ablation of the essential core subunit Ndufs2 subunit of complex I in DA neurons are sufficient to produce progressive, L-DOPA-responsive parkinsonism [82]. The gene discussed is NDUFS2; the disease is Parkinson disease.