Given the previously reported effects of GCPII inhibition in preserving nerve structure and function in models of chemotherapy-induced neurotoxicity and diabetic neuropathy [37,38] and the significant increase in GCPII expression in Schwann cells following nerve injury, we next aimed to investigate whether inhibiting GCPII would benefit nerve regeneration, specifically focusing on myelination. The gene discussed is FOLH1; the disease is diabetic neuropathy.