Osteocytes respond to PTH by lowering sclerostin expression and secretion, increasing osteoblast bone formation activity.(13) When chronically elevated, as seen in CKD, PTH increases osteocyte‐derived receptor activator of nuclear kappa‐B ligand (RANKL), leading to increased osteoclast differentiation and bone resorption.(14) In rodents, these bone formation and resorption events primarily occur near bone surfaces, making the periosteal surface a promising location to detect matrix changes in CKD with high PTH and following calcimimetic treatment. Here, TNFSF11 is linked to chronic kidney disease.