In the light of KDM6A’s ability to repress PPARγ expression and activity [25] and given the link between PK2 and KDM6A here shown, it can be hypothesized that the PK2 modulation of PPAR gene expression could be epigenetically mediated by histone demethylases in the spinal cord of BTZ-induced neuropathy suffering mice. The gene discussed is KDM6A; the disease is neuropathy.