Glycerophospholipids (PLs) play pivotal roles in our body as main structural components of biological membranes and precursors of lipid mediators. Recently, we revealed that peripheral nerve injury (PNI) increased arachidonic acid-containing PLs (ARA-PLs) in the dorsal root ganglion (DRG), spinal microglia, and spinal astrocytes. Therefore, we focused on LPCAT3 (also called LPLAT12), a biosynthetic enzyme of ARA-PLs, and established cell type-specific Lpcat3-knockout mice: DRG neuron (Advillin^Cre), macrophage/microglia (Cx3cr1^CreERT2), and satellite glia/astrocyte (Gfap-Cre). We found that PNI-induced mechanical allodynia were attenuated in DRG neuron-specific and satellite glia/astrocyte-specific Lpcat3-knockout mice. These results suggest that alteration of quality of lipid in these cells may be a cause of neuropathic pain. Now, we are analyzing the mechanisms by which ARA-PLs are involved in neuropathic pain.