Although these models have led to huge advances in our understanding of PD—implicating mitochondrial dysfunction, oxidative damage, and protein handling systems in pathogenesis—they typically either fail to recapitulate the gradual nature of this degenerative disease or lack the defining pathology (e.g., Parkin and α-synuclein transgenic mice fail to show progressive nigrostriatal degeneration, although rotenone-treated mice do show Lewy bodies (intracytoplasmic inclusions that are composed primarily of α-synuclein and ubiqutin)) [3,4]. The gene discussed is PRKN; the disease is Parkinson disease.