Nevertheless, over recent years, new approaches aimed to address osteoporosis have largely focused on osteotherapeutics designed to directly target RANKL or OPG, or indirectly effect this signaling pathway via anti‐sclerostin or anti‐cathepsin K approaches, for example.[124, 125] To the best of our knowledge, this is first evidence of an intervention that drives against bone loss by contributing to a reduction in the expression of RANK. This evidence concerns the gene TNFRSF11A and osteoporosis.