Denosumab is known to bind to RANKL, inhibiting the formation, function, and survival of osteoclasts; reducing bone resorption; and increasing bone mass, which leads to a smaller amount of calcium released from the bones, eventually causing hypocalcemia, followed by affecting the parathyroid gland, thus contributing to reduced phosphorus (Bekker et al., 2004; Evenepoel et al., 2014). This evidence concerns the gene TNFSF11 and Hypocalcemia.