STAT3 and non-small cell lung carcinoma: 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.