About 50–65% of patients with EGFR-mutated NSCLC respond to EGFR tyrosine kinase inhibitors (TKIs), [16] but most patients become resistant to these treatments by acquiring a secondary point mutation in EGFR or activation of additional signaling pathways, including mesenchymal-epithelial transition factor (MET) and KRAS [17, 18]. This evidence concerns the gene KRAS and non-small cell lung carcinoma.