Oxaliplatin-induced peripheral neuropathy (OIPN) is one of the side effects of oxaliplatin chemotherapy. In addition, most currently available analgesic drugs lack efficacy against OIPN. Using the FDA-Adverse Event Reporting System, we previously identified that the HMG-CoA reductase inhibitors statins have the potential to ameliorate OIPN, although the underlying mechanism is still unknown. In this study, we reveal the possible mechanism of statin, via glutathione S-transferase (GST) in dorsal root ganglion (DRG), to investigate therapeutic drugs for OIPN. Following the administration of oxaliplatin, mice demonstrated a cumulative dose-dependent decrease in paw withdrawal threshold (PWT). The decrease in PWT by oxaliplatin was ameliorated on day 7 in mice orally administered atorvastatin, simvastatin, and rosuvastatin and lasted for 21 days. Our previous reports assessing a gene-related database revealed that the expression of GST family members is regulated by statins. Oxaliplatin-induced cell death in PC12 cells was inhibited by treatment with each statin for 24 hours. In addition, transfection of Gstm1 siRNA into PC12 cells reverted the protective effect of statins. These results suggest that the increment of GST in DRG induced by statin might be novel therapeutic oxaliplatin-induced chronic neuropathy.