TGFB1 and cranioectodermal dysplasia: This mutation results in a similar bone defect in mice (CED mice).8 However, TGF-β1 is unable to induce osteogenesis in mesenchymal pluripotent cells, but increases the pool of osteoprogenitors by inducing chemotaxis and proliferation.8 Apoptosis of osteoblasts is also blocked by TGF-β1 deletion through maintenance of survival during transdifferentiation into osteocytes.29 In addition, TGF-β treatment blocked osteoblast mineralization in culture,30 indicating its bi-functions in osteoblast differentiation.