The combination of a lower 25‐hydroxyvitamin D (25(OH)D) conversion rate and reduced calcium reabsorption and phosphate excretion from the renal tubules leads to hypocalcaemia, hyperphosphatemia, and hypercalciuria, whereas the lack of PTH itself results in reduced bone turnover and bone disease.(1) Conventional therapy is based on supplementation with oral calcium salts and active vitamin D, but this often fails to normalize biochemical parameters other than serum calcium. The gene discussed is PTH; the disease is Hypercalciuria.