Conversely, sensory neuron activity generated from the ectopic lesion site (Chen et al., 2016) may cause overexpression of FKN from primary afferent neurons or spinal dorsal horn neurons and result in microglia activation via the CX3CR1/p38-MAPK pathway (Figure 9; Clark et al., 2007a; Xu et al., 2007; Crown et al., 2008); and this has been suggested to play roles in microglial activation and the persistence of neuropathic pain in models of peripheral nerve injury (Zhuang et al., 2007; Zhang et al., 2015). This evidence concerns the gene CX3CR1 and peripheral nerve injury.