The bone phenotype in most patients with Eiken syndrome (i.e., delayed ossification) points toward a gain-of-function effect on PTHrP/PTH1R-mediated signaling in the growth plate, as it is well established that this signaling response acts normally to sustain growth plate chondrocyte proliferation and to delay the differentiation of these cells toward the hypertrophic state. The gene discussed is PTH1R; the disease is Eiken syndrome.