Based on the potential pathogenesis of osteoporosis by proteomics analysis for osteoporosis samples and experiments in biochemistry and molecular biology, we demonstrated that TRAF6 could be degraded by REGγ via ubiquitin/ATP (Adenosine Triphosphate)-independent degradation manner directly and the dephosphorylation of NIP30 modulated by the inhibitor of CKII TTP22 promoted the degradation of TRAF6 by REGγ-20S proteasome to postpone osteoporosis. The gene discussed is CSNK2A1; the disease is osteoporosis.