With reference to EGFR mutations, vast literature data emphasize the link between EGFR axis hyperactivity and VEGF (vascular endothelial growth factor) induction and upregulation, as well as VEGFR (vascular endothelial growth factor receptor)-EGFR synergy, in promoting tumor growth, thus providing a strong preclinical background for the potential benefits of antiangiogenic monoclonal antibody plus EGFR-tyrosine kinase inhibitor combinations in this subset of patients[4-6]. This evidence concerns the gene VEGFA and neoplasm.