The spectrum of resistance mechanisms that arise following amivantamab are likely to be different compared with EGFR kinase inhibitors, and can be speculated to include changes in cell surface EGFR or MET expression, mutations in other compensatory receptors including HER2 and PDGFRA or pathway alterations further downstream including RAS mutations, such as those seen in colorectal cancers with acquired resistance to cetuximab [65,94]. This evidence concerns the gene EGFR and colorectal cancer.