Proteomic analysis of the conditioned medium from RT4 (BC) cells identified IL-8, vascular endothelial growth factor-A (VEGF-A), and tissue inhibitor of metalloproteinase-1 (TIMP-1), which may have contributed to HUVEC activation, and this was validated in vitro by blocking either IL-8 or VEGF-A, which dampened HUVEC activation [5]. The gene discussed is CXCL8; the disease is breast cancer.