It is reported that PD features such as α-syn aggregation and tau hyperphosphorylation induced by rotenone could be reversed by GSK-3β, and at the same time, α-syn regulates GSK-3β activity by decreasing Ser9 phosphorylation and elevating Tyr216 phosphorylation to mediate the neurotoxicity [30, 31]. The gene discussed is GSK3B; the disease is Parkinson disease.