Substantial progress has been made in recent years in the study of CNP and their role in skeletal disorders, particularly achondroplasia, which is caused by a gain-of-function mutation in FGFR3 that results in constitutive activation of FGFR3 and the downstream MEK/ERK MAPK pathway [70,71]. The gene discussed is MAP2K7; the disease is achondroplasia.