In the adult study, these changes have been independently associated with the disease and it has been hypothesized that serum RANKL levels are lower because of a shift of circulating RANKL to LCH lesions with a concomitant increase in its cell-bound concentrations, and a compensatory increase of OPG levels [20]. The gene discussed is TNFRSF11B; the disease is Langerhans cell histiocytosis.