This conclusion is underlined by the fact that the osteoporotic phenotype in TNF-α transgenic mice cannot be combated with an anti-TNF-α treatment, but by sclerostin-inhibition, pointing out the importance of the RANKL–OPG balance in the pathophysiology of these models as well as in human osteoporosis. The gene discussed is TNFSF11; the disease is osteoporosis.