The present study demonstrated that CaMKII, but not MAPKs, has an important role in cPLA2-dependent tactile allodynia via the regulation of phosphorylation and translocation of cPLA2, both of which are mediated by P2X3R/P2X2+3R and voltage-dependent Ca2+ channels in primary afferent neurons following peripheral nerve injury. This evidence concerns the gene CAMK2G and peripheral nerve injury.