The phenotype of the Trpc1–/– mice is consistent with that of FHH in humans, and the possibility that mutations in the TRPC1 gene may be a cause of hypercalcemia in some patients with FHH who did not have CASR, GNA11, or AP2S1 mutations was therefore explored. This evidence concerns the gene CASR and familial hypocalciuric hypercalcemia.