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. The gene discussed is GNA11; the disease is familial hypocalciuric hypercalcemia.