In addition, activation of STAT3 (signal transducer and activator of transcription 3) has been reported to promote NSCLC development, which can be stimulated by either receptor tyrosine kinases (EGFR, VEGFR) or non-receptor tyrosine kinases (JAKs, c-SRC), leading to angiogenesis and cell survival events [29]. This evidence concerns the gene NTRK1 and non-small cell lung carcinoma.