Conversely, germline loss-of-function CaSR and Gα 11 mutations lead to the opposite phenotypes of familial hypocalciuric hypercalcemia (FHH) types 1 and 2, respectively (1, 2), which is characterized by lifelong elevations of serum calcium concentrations in association with normal or mildly raised serum PTH concentrations, and low urinary calcium excretion (calcium‐to‐creatinine clearance ratio < 0.01) (13, 14). This evidence concerns the gene CASR and familial hypocalciuric hypercalcemia.