It is possible to find a precise therapeutic target to compensate for the haploinsufficiency of Runx2 in CCD based on the transcriptional regulation and pre- and post-translational modification of Runx2. For example, NELL1, a key functional mediator of Runx2 osteogenic activity, rescues calvarial defects in Runx2+/− mice42. Here, RUNX2 is linked to cleidocranial dysplasia 1.