Given that KCR mainly exerts promoting transcription effects, we speculate that after peripheral nerve injury, the elevated KCR levels in macrophages may induce pain by upregulating the expression of pain-causing genes, and reduced KCR levels in the sensory neurons may contribute to pain genesis by downregulating the anti-nociceptive genes, such as GABA receptors or potassium channels encoding genes (4, 32). This evidence concerns the gene CLEC4F and peripheral nerve injury.