It was reported that breast cancer cells stimulated CCL5 secretion by MSCs, and CCL5 in turn induced tumor cell migration and promotes invasion and metastasis.42 While human and mouse MSCs routinely express low levels of selected chemokines and receptors,43, 44 we show that TNF-α-pretreated hMSCs is sufficient to drive the paracrine CCL5-mediated activation of EMT program and metastasis in cancer cells. The gene discussed is CCL5; the disease is breast carcinoma.