As discussed above, FGF-2 coordinates with fibronectin to support breast cancer dormancy (92–94), but adding IL-6, IL-8, or transforming growth factor β1 (TGF-β1) to that system disrupts dormancy, providing evidence toward inflammation-stimulated reactivation from dormancy in bone marrow (95). This evidence concerns the gene TGFB1 and breast carcinoma.