Osteogenesis imperfecta (OI) is the most common genetic form of brittle bone disease and results in defects of both bone and connective tissue. OI patients can have significant problems with mobility due to joint dysfunction due in part to tendinopathy. In a new study published in the journal Proceedings of the National Academy of Sciences, researchers at Baylor College of Medicine identify a protein signaling mechanism driving this dysfunction and find that inhibiting this signaling pathway can prevent onset of tendinopathy problems in mouse models.