Background　K+?蛳Cl- cotransporter 2（KCC2） is an important member of the cation?蛳chloride cotransporter （CCCs） family， its expression or ion transport activity downregulation can cause disinhibition of GABAergic neurons through altering intracellular Cl- stability of nerve cells， amd ultimately induce the hypersensitivity to noxious stimuli， namely hyperalgesia. Brain-derived neurotrophic factor/tyrosine kinase receptor B（BDNF/TrkB） signaling pathway can regulate the protein expression and ion transport activity of KCC2， indicating that BDNF/TrkB signaling pathway may be involved in the occurrence of hyperalgesia. Currently， scientists have found that BDNF/TrkB signaling pathway blockers and KCC2 agonists are able to relieve or prevent neuropathic pain and inflammation induced hyperalgesia.　Objective　To investigate the role of KCC2 in the occurrence and development of hyperalgesia.　Content　Reviewing the relationship between KCC2 and hyperalgesia.　Trend　To provide new ideas for the prevention and therapy of hyperalgesia.