There are a wide range of resistance mechanisms to EGFR inhibition identified, but in NSCLC it is mainly due to the acquisition of the EGFR T790M gatekeeper mutation (~ 60%) in the ATP binding pocket of the EGFR kinase domain, with the second most common resistance mechanism being the amplification of the hepatocyte growth factor receptor (MET) gene (10–20%) [17]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.