Previous studies using LPA receptor 1 (LPA1)-KO mice have revealed that pain-related phenotypes are completely abolished in animal models of pain [5,6,7], including the following: hyperalgesia in neuropathic pain (NeuP), such as partial sciatic nerve ligation (pSNL); chemotherapeutic agent paclitaxel-induced models; type-1 and type-2 diabetes-related models; the central poststroke pain model. This evidence concerns the gene LPAR1 and type 2 diabetes mellitus.