While the previous study demonstrated enhanced peripheral expression of GSK3β in PD patients, the present data show a significant reduction in GSK3β levels in PD PBMCs.28 Moreover, Marksteiner et al indicated remarkable decrease in GSK3β levels in PBMCs of patients with MCI and AD, which is consistent with our result.29 Collectively, our results confirmed the peripheral mitochondria dysfunction in PD and suggest that PGC1α, TFAM and GSK3β down‐regulated levels could be demonstrative of events taking place in PD pathogenesis. This evidence concerns the gene GSK3B and Parkinson disease.