TGFB1 and bone fracture: However, our data revealed that abundant endogenous TGF‐β1 is secreted in fractured microenvironment and is sufficient to trigger TGF‐β signalling regulating periosteal progenitor cell differentiation and endochondral bone formation, implicating exogenous TGF‐β1 as a potential treatment for fracture patients, especially for those with deficiency of TGF‐β pathway related molecules.