Biochemical changes in this condition reflect a disordered bone‐related endocrine environment initiated by declining serum calcium levels causing secondary hyperparathyroidism.20 Although the PTH‐induced rise in 1,25(OH)2D improves intestinal calcium absorption, it also inhibits osteoid mineralization,21, 22 thus contributing to hyperosteoidosis. The gene discussed is PTH; the disease is secondary hyperparathyroidism.