These results further suggest that ADAM8 may be a therapeutic target for blocking inflammatory bone destruction.(1) Increased expression of ADAM8 enhances OCL formation, differentiation, and bone resorption per OCL and results in osteopenia in vivo, whereas loss of ADAM8 in vivo does not significantly affect normal bone homeostasis but blocks the OCL stimulatory effects of inflammatory cytokines such as TNF-α, which is a major cytokine implicated in inflammatory bone loss.(25). The gene discussed is ADAM8; the disease is Osteopenia.