Therefore, we hypothesized that abnormal mineral metabolism, such as hypercalcemia and hypercalciuria observed in untreated HPP, might facilitate the development of nephrocalcinosis rather than an inflammatory response associated with TNAP deficiency.(72) This study was terminated at 70 dpn; therefore, long‐term effects of AAV8‐TNAP‐D10 with the presence of age‐related ectopic calcifications remain unknown but are an area for further study. The gene discussed is ALPL; the disease is hypophosphatasia.