The rationale for this approach stands on the excessive TGF-β signaling found in the skeleton of three severe OI mouse models (Col1a2+/G61°C, Crtap−/− and Col1a1Jrt/+), and the concomitant rescue of the pathological bone phenotypes by using 1D11, a specific anti-TGF-β monoclonal antibody in two of them, Col1a2+/G61°C, Crtap−/− (Grafe et al., 2014; Greene et al., 2021). The gene discussed is COL1A2; the disease is osteogenesis imperfecta.