STAT3 dimers eventually translocate into the nucleus and trigger the transcription of genes associated with a series of cancer hallmarks, including proliferation, apoptosis, angiogenesis, and immune evasion.[41] Non-receptor tyrosine kinases, such as SRC, can also activate the JAK/STAT3 signaling pathway.[42] In samples from NSCLC patients and cell lines, persistent STAT3 activation can be observed, and high expression of intratumoral phosphorylated STAT3 correlates with an advanced disease stage and EGFR mutation. This evidence concerns the gene NTRK1 and cancer.