Yamanaka et al. previously reported the potential effect of circulating CNP on craniofacial hypoplasia using Fgfr3ach/SAP-Nppc-Tg mice, crossed Fgfr3ach mice with transgenic mice in which CNP is expressed in the liver under the control of the human serum amyloid-P component promoter, resulting in elevated levels of circulatory CNP [17]; this is the first report that demonstrate the therapeutic potential of CNP for the treatment of foramen magnum stenosis and midfacial hypoplasia in achondroplasia. Here, CNP is linked to achondroplasia.