In addition to TME-mediated effects, the chemokines may also regulate the intrinsic prometastatic activities of the cancer cells, as suggested by recent studies in breast cancer, demonstrating that the prometastatic chemokine CCL5 promoted the metabolic activity of the cancer cells; stimulation of the cancer cells by this chemokine has led to increased glycolysis-dependent tumor growth and invasion in vitro and to elevated ability to form tumors in vivo [61,62]. The gene discussed is CCL5; the disease is breast cancer.