For example, a subset of CAFs is able to drive tumour progression through integrin α11-mediated promotion of CAF invasion and CAF-induced tumour cell invasion via the production of the pro-invasive matrix protein tenascin C.30 Furthermore, in breast cancer, a CD146+-fibroblast population could preferentially increase metastasis associated with the deposition of a number of ECM components found in clinically aggressive disease.31 An analysis of lymph node metastases from breast cancer patients identified divergent CAF subsets that were similar to those found in primary tumours. The gene discussed is MCAM; the disease is neoplasm.