More importantly, double heterozygotes for Twist1 and Runx2 deletion have none of the skull abnormalities observed in single-mutant mice (Bialek et al., 2004), which supports the notion that Twist1+/− haploinsufficiency promotes Runx2 activity and leads to the premature osteogenic differentiation of suture MSCs, ultimately resulting in craniosynostosis. Here, RUNX2 is linked to craniosynostosis.