Tumor cells take advantage of myeloid cells to maintain tissue homeostasis by exploiting the myeloid cells' capacity to produce inflammatory mediators [e.g., interleukin-6 [IL-6] and tumor necrosis factor-α [TNF-α]], growth factors that affect tumor proliferation and vessel formation [e.g., transforming growth factor-β [TGF-β] and vascular endothelial growth factor [VEGF]], and enzymes that degrade matrix proteins [e.g., matrix metallo-proteinases [MMPs]] (3, 4). The gene discussed is VEGFA; the disease is neoplasm.