AuthOr’s VIew AuthOr’s VIew

In normal cells and under physiological conditions, the binding of various cyto-kines to their receptors rapidly and tran-siently activates signal transducer and activator of transcription 3 (STAT3). STAT3 is negatively regulated by various proteins, such as suppressor of cytokine signaling (SOCS) and protein inhibitor of activated STAT (PIAS). When con-stitutively activated, STAT3 promotes malignant transformation.1 Accordingly, somatic mutations in the Src homology 2 (SH2) domain of STAT3 are frequently found in large granular lymphocytic leu-kemia.2 Furthermore, mutations in Janus kinase 2 (JAK2) that result in constitutive STAT3 activation have also been identified in myeloproliferative disorders.3 However, similar mutations in the JAK/STAT3 pathway have not been reported in lung cancer patients. To date, several driver oncogenes, including Kirsten rat sarcoma viral onco-gene homolog (KRAS), epidermal growth factor receptor (EGFR), and anaplastic lymphoma kinase (ALK), have been iden-tified in non-small cell lung carcinoma (NSCLC), a common type (accounting for 80 % of all cases) of lung cancer. Formerly, STAT3 was thought to act in pathways Involvement of STAT3 in immune evasion during lung tumorigenesi