Studies have revealed EGFR to be upregulated in 60–80% of colorectal malignancies.49 Clinical evaluations frequently utilize immunohistochemistry (IHC) assays to identify patients with CRC expressing EGFR in at least 1% of the tumor cells.50 The activation of EGFR sets off a cascade of intracellular signaling, prominently involving the MAPK and PI3K/Akt pathways, which are known to augment cellular proliferation, inhibit apoptosis, and promote angiogenesis.51 This evidence concerns the gene EGFR and colorectal carcinoma.