EGFR can be aberrantly activated through mutations or amplification/overexpression, which drives pro-tumor effects in cancers such as non-small cell lung cancer, pancreatic cancer and head and neck cancer, leading to approval of EGFR targeted therapies including tyrosine kinase inhibitors (TKI’s) gefitinib, erlotinib, afatinib, dacomitinib, osimertinib, and vandetanib, and the monoclonal antibodies cetuximab, panitumumab and necitumumab (1, 2, 10-13). This evidence concerns the gene EGFR and cancer.