Similarly, resistance to cetuximab has been reported in colorectal cancer and head and neck cancer, causing low objective response rates Primary and acquired resistance have been associated with many aspects of cetuximab’s biology, including receptor internalization, genetic polymorphisms in the EGFR gene and mutations in the KRAS gene, affecting both the ability of cetuximab to block EGFR-mediated signal transduction and ADCC [69,70]. This evidence concerns the gene EGFR and colorectal cancer.