Using the GlatmTg(CAG‐A4GALT) Fabry mouse model with impaired mTAL, we demonstrated that mTAL dysfunction, ie, a decrease in blood Ca2+, induces an elevation in the levels of phosphaturic hormone PTH and that, ultimately, secondary hyperparathyroidism results in accelerated bone resorption and subsequent hypercalcemia18 and hyperphosphatemia, followed by hypercalciuria18 and hyperphosphaturia, thereby causing osteomalacia. Here, PTH is linked to secondary hyperparathyroidism.