Biologically, altered tumor angiogenesis as a way to escape cetuximab antitumor activity has been previously reported in CRC cellular models and ascribed to either VEGF protein overexpression or increased VEGFR-1 and VEGFR-2 activation [126, 127]; taken together, these findings suggest that increased expression of pro-angiogenic ligands and cognate receptors (including VEGFs, VEGFRs, and Eph receptors) may dictate sensitivity to anti-EGFR therapy in colorectal tumors. This evidence concerns the gene EGFR and colorectal neoplasm.