In the early 1980s the EGFR pathway was pointed to as a potential target for cancer therapy [7,8] and two anti-EGFR strategies were adopted: monoclonal antibodies (Mabs) which bind the extracellular domain, interfering with the natural ligand, and low-molecular-weight tyrosine kinase inhibitors (TKIs) which interfere with ATP for the tyrosine kinase domain [9]. Here, EGFR is linked to cancer.