Currently, there is a general consensus that MIF promotes tumor growth by several mechanisms; it stimulates cancer cell proliferation by triggering the MAPK/PI3K/Akt pathways, inhibits induction of p53-dependent apoptosis, increases production of vascular endothelial growth factor (VEGF) and inhibits the antitumor immune response (4–6). This evidence concerns the gene VEGFA and neoplasm.