Although IFNγ directly inhibits osteoclastogenesis by interfering with the RANKL-RANK signaling pathway and inducing apoptosis mediated by Fas/Fas ligand signaling [27, 66], accumulating evidence suggests that Th1-derived IFNγ and TNFα induced by acquired immune response promote net bone loss in pathological conditions such as periodontitis [28, 67–70]. The gene discussed is TNFRSF11A; the disease is periodontitis.