Although it seems plausible that the relatively modest changes in PTH ligand affinity and potency that we observed for the PTH1R‐R186H mutant in vitro could translate into the PHP1B‐like phenotype of hypocalcemia and hyperphosphatemia seen in the patients with this homozygous mutation, firmer support for this hypothesis will likely require additional in vivo or clinical evaluation. This evidence concerns the gene PTH and hyperphosphatemia.