It was previously suggested that the delayed ossification seen in Eiken syndrome patients with the PTH1R-R485X variant might arise from an impaired capacity of the mutant receptor to activate the Gαq/phospholipase C (PLC)/inositol triphosphate (IP3)/intracellular calcium (iCa2+) signaling7. The gene discussed is GNAQ; the disease is Eiken syndrome.