In the early 80s the EGFR was pointed out as a potential target for cancer therapy [12] 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, which interfere with the tyrosine kinase domain [13]. The gene discussed is EGFR; the disease is cancer.