With regard to the cellular mechanisms whereby TN-C mediate its effects, a study using human mammary fibroblasts as a model of breast cancer-associated fibroblasts (CAFs) suggests that TN-C treatment increased collagen gel contraction and increased synthesis of TN-C and integrin αvβ1, in turn leading to increased TGF-β activation [57]. The gene discussed is TGFB1; the disease is breast cancer.