Given the aforementioned beneficial effects of TGF‐β inhibition on the fracture resistance of bones in WT mice and upregulation of TGF‐β signaling in patients with OI, there is potential for a disease‐specific mechanism by which an anti‐TGF‐β blocking antibody can prevent or reduce the number of fractures in patients with OI. The gene discussed is TGFB1; the disease is osteogenesis imperfecta.