Early on in the clinical development of EGFR-tyrosine kinase inhibitors (EGFR-TKIs), which targeted this pathway, it was realized that patients whose tumor harbored an activating mutation in the EGFR gene at exons 19 and 21 had more dramatic responses and better clinical outcomes than their EGFR wild-type (W/T) counterparts (7, 8). This evidence concerns the gene EGFR and neoplasm.