For example, a phase IIb study involving 5 patients with ADH1 showed that i.v. administration of NPSP795 (an amino‐alcohol calcilytic compound) at doses ranging from 5 to 30 mg, increased PTH, but did not significantly alter ionized blood calcium concentrations.(23) We have further evaluated the efficacy of NPSP795 treatment for ADH1 by undertaking in vitro and in vivo studies involving Nuf mice, which have hypocalcemia (Table 1) in association with a germline gain‐of‐function CaSR mutation, Leu723Gln. This evidence concerns the gene CASR and Hypocalcemia.