Although the molecular mechanisms that link RANKL and OPG with glucose metabolism have not yet been fully elucidated, systemic or hepatic inhibition of RANKL signaling in a mouse model of T2DM ameliorated hepatic insulin resistance (IR), one of the main pathogenic key factors of T2DM, and markedly improved serum glucose concentrations [37]. The gene discussed is TNFRSF11B; the disease is type 2 diabetes mellitus.