Camurati–Engelmann disease (CED) is driven by activating mutations in TGF-β1,480 leading to diaphyseal osteosclerosis, thickened long bones, bone pain, and muscle weakness.481 Excessive TGF-β1 activity induces enthesopathy,482 characterized by vascular hyperplasia, bone degeneration, and fibrocartilage calcification. This evidence concerns the gene TGFB1 and enthesopathy.