Since the expression and release of Rankl is not altered in MLII osteoblasts, it is likely that increased levels of Il-6 induce osteoclastogenesis in MLII mice by Rankl-independent mechanisms (Kudo et al, 2003) in agreement with pro-osteoclastogenic functions of Il-6 in transgenic mice which display osteopenia and increased osteoclastogenesis (De Benedetti et al, 2006), and Il-6-deficient mice which are protected from ovariectomy-induced bone loss (Poli et al, 1994). This evidence concerns the gene IL6 and Osteopenia.