A previous study has demonstrated that dominant-negative Mek1 expression in osteoblasts results in CCD in mice, while constitutively-active Mek1 expression in osteoblasts partially rescues CCD phenotypes caused by Runx2 haploinsufficiency [5], suggesting that the MEK-ERK MAPK pathway regulates RUNX2 in osteoblasts. This evidence concerns the gene RUNX2 and cleidocranial dysplasia 1.