Since LPI bound to G-protein coupled receptor 55 (GPR55) and dysregulated LPI‒GPR55 signaling results in metabolic diseases [190], treatment of monocytes and pre-osteoclasts with either LPI or a GPR55 agonist, O-1602, induces osteoclastogenesis through osteoclast differentiation/polarization and bone resorption activity in vitro [191]. The gene discussed is GPR55; the disease is Other metabolic disease.