For instance, osteocytes can produce sclerostin (Sost), which inhibits bone formation and receptor activator of nuclear factor-κB ligand (Rankl), which promotes bone resorption.49,62 Osteocytes also express Fgf23, which is linked to hypophosphatemia and impaired bone mineralization in autosomal-dominant hypophsophatemic rickets/osteomalacia (ADHR), X-linked hypophosphatemic rickets/osteomalcia (XLH), and tumor-induced osteomalacia (TIO).63–65 The proinflammatory cytokines tumor necrosis factor alpha (Tnf-α) and interleukin 1β (IL-1β) expressed by osteocytes can upregulate Fgf23. This evidence concerns the gene TNFSF11 and autosomal dominant hypophosphatemic rickets.