Here, aiming at providing not only novel molecular targets for future osteoporosis treatment, but also effective pharmaceutical remedies to inhibit osteoclastogenesis, we previously screened several drugs and found that Hes could attenuate RANKL-induced osteoclastogenesis by regulating Irf-3 mediated activation of Jnk, c-Jun and NFATc-1 in osteoclasts, thereby extending the spectrum of translational osteoporosis treatment on both the pharmaceutical and molecular levels. This evidence concerns the gene JUN and osteoporosis.