Primary EGFR-TKI resistance has been reported to be related to v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations,[21] phosphoinositide-3-kinase catalytic alpha (PIK3CA) mutation,[22] de novo proto-oncogene MET amplification,[23] Bim deletion polymorphism,[24] phosphatase and tensin homolog (PTEN) loss,[25] and de novo T790M mutation of the EGFR gene.[26] Our study may provide another evidence that low content of mutant EGFR DNA in lung cancer tissues may cause primary resistance to EGFR-TKI therapy in NSCLC patients with exon 19 deletions and exon 21 L858R EGFR mutations. This evidence concerns the gene MET and non-small cell lung carcinoma.