The TGF‐β signaling pathway was shown to be significantly elevated in the bones of both recessive CRTAP and dominant G610C OI mouse models compared with WT mice, and this elevation contributed to the high bone turnover and low bone mass observed in these OI models.(12) Both of these mouse models respond to 1D11therapy, with increases in vertebral and femoral trabecular bone volume fraction (BV/TV) and bending strength of femur mid‐shafts in the CRTAP mouse model.(12) In contrast, in the more severe model, Col1a1Jrt/+, the same effects were not observed. This evidence concerns the gene TGFB1 and osteogenesis imperfecta.