Increasing evidence has shown that noxious stimuli alter the expression of epigenetic regulators and relevant epigenetic modifications, resulting in the dysregulation of pain‐related genes.[1, 6, 35, 36] For example, G9a, a histone methyltransferase, was reported to promote the downregulation of potassium channels and opioid receptors genes after nerve injury.[37, 38] Another histone methyltransferase, EZH2, was also found to stimulate proinflammatory cytokines secretion in neuropathic pain.[39, 40] Additionally, HDAC activity was found to decline in neuropathic pain model.[41]. This evidence concerns the gene EZH2 and injury.