TGFB1 and cranioectodermal dysplasia: Therefore, these two missense mutations (near the cysteine residues involved in LAP dimerization) enhance TGFβ1 effects on both osteoblasts and osteoclasts, increasing bone turnover.(6) Accordingly, CED mutations are gain-of-function defects for the skeleton.(75) TGFβ1 can inhibit some myogenic transcription factors and adipogenesis,(76,77) perhaps explaining the weakness and cachectic phenotype of severe CED.(27)