A number of independent studies researching into the mechanisms underlying the anti-tumor activities of ES have shown that the drug restrains tumor growth through various channels, including repressing combination between vascular endothelial growth factor (VEGF) and endothelial cells (ECs), initiating EC apoptosis [3], and bonding to cell surface receptors such as nucleolin [4] to regulate a myriad of signaling cascades. This evidence concerns the gene CD177 and neoplasm.