However, the literature indicates that the response to this drug may vary depending on the TNAP mutation.(50, 51, 52) Monoclonal anti‐sclerostin antibody treatment has been demonstrated to reduce bone resorption and stimulate bone formation, increasing the BMD in HPP patients.(45) Bisphosphonates and calcium and/or vitamin D3 have been used to treat HPP; however, bisphosphonate treatment in adult HPP may increase the risk of fracture,(53, 54, 55) as these are analogs of PPi and therefore contribute to the inhibition of HA formation. The gene discussed is ALPL; the disease is hypophosphatasia.