It has been demonstrated that activation of LXRs by GW, a synthetic full agonist for both LXRα and LXRβ isoforms, which can readily cross the blood-brain barrier to exert its specific actions in brain, exerted an antinociceptive effect in rat joint pain and diabetes-caused thermal hyperalgesia [38, 39], suggesting that the dysfunction of LXRs contributes to pain pathogenesis. The gene discussed is NR1H3; the disease is diabetes mellitus.