Overexpression of miR-125a restricted osteoclastogenesis because miR-125a targets TRAF6, whereas the transcription of miR-125a was negatively regulated by the binding of NFATc1 to the promoter of miR-125a, suggesting the existence of a TRAF6/NFATc1/miR-125a regulatory feedback loop.184 In a CIA rat model, miR-125a treatment effectively attenuated arthritis severity.185 Moreover, miR-146 was reported to blunt TLR and cytokine signaling by base-pairing with sequences in the 3′ UTRs of TRAF6.119. The gene discussed is TRAF6; the disease is arthritic joint disease.