The majority of EGFR kinase domain mutations are found at exons 18 to 21, which increases EGFR’s kinase activity and triggers over activation of downstream signaling pathways, the three major downstream signaling pathways such as phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR, interleukin 6(IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3), mitogen-activated protein kinases (MAPK)/extracellular signal-regulated kinases (ERK) which supports tumorigenesis of NSCLC (3, 136). This evidence concerns the gene STAT3 and non-small cell lung carcinoma.