In 2001, an unexpected skeletal phenotype of rickets was presented in CaSR-absent mice, indicating that calcium-sensing receptor was present in the skeleton and its absence resulted in the defective mineralization of cartilage and bone.1 However, the lack of apparent skeletal defects in global CaSR−/− and PTH−/− mice indicated a bone disorder resulted from the direct effects of PTH.17–19 Recent studies have focused on the function of CaSR in both the chondrocytes in growth plates and osteoblast-lineage cells. This evidence concerns the gene PTH and rickets.