We also found that, although the c-Met/β1 integrin complex induced the expression of mesenchymal genes and pathways associated with metastases independent of the breast cancer’s ER/PR/Her2 receptor status, the complex formation only increased intravasation in triple-negative breast cancers, because the low baseline level of intravasation in luminal A ER+PR+HER2– cells could not be enhanced by c-Met/β1 complex formation. The gene discussed is MET; the disease is breast carcinoma.