Additionally, CCL5 was demonstrated to promote chemotaxis of monocytes, increasing MMP9 expression in MCF7 cells [40] and angiogenesis, partly dependent on vascular endothelial growth factor (VEGF) secretion by endothelial cells [41], suggesting that the expression of CCL5 by cancer cells results not only in monocyte migration to the tumor site but also in protumorigenic activities of this chemokine and of proinflammatory cytokines that may facilitate metastasis formation and contribute to disease progression. The gene discussed is VEGFA; the disease is cancer.