The peritrabecular fibrosis has been regarded as the key indicator of high‐turnover bone diseases (eg, osteitis fibrosa) when fibroblast‐like cells produce much irregularly organized extracellular matrix in response to persistently increased PTH levels.(53) Bone pathologies mediated by hyperparathyroidism and elevated turnover are characterized by active remodeling in both bone formation and resorption.(54) Given the fact that our patient had normal functioning parathyroid and her osteoblastic osteogenesis was low, the histological manifestation in our case seems to be irrelevant. The gene discussed is PTH; the disease is osteitis fibrosa.