Data from these studies indicate that anti-EGFR/VEGFR2 BsAb elicited more comprehensive anti-tumor activity via multiple mechanisms of action, including direct inhibition of EGFR and VEGFR2 in TNBC cells, and disruption of autocrine and paracrine pathways in TNBC and endothelial cells, compared to the individual parental mAbs. The gene discussed is EGFR; the disease is neoplasm.