The observed superior antitumor potency of GC1118 over cetuximab against CRC PDXs harboring activating KRAS mutations could be due to the strong inhibitory activity of the interaction between EGFR and high-affinity EGFR ligands [8,20,21], providing a rationale for clinical application of the expression pattern of EGFR ligands as a novel biomarker predictive of the response to GC1118 in treating patients with refractory mCRC. This evidence concerns the gene KRAS and colorectal carcinoma.