STAT3 and non-small cell lung carcinoma: Since the expression of STAT3 transcriptional targets but not STAT3 itself significantly correlates with SIL IC50 of five NSCLC cell lines, we conclude that external and/or constitutive activation of STAT3, for example, due to gain-of-function mutations or enhanced upstream signaling (e.g., tyrosine kinase receptors, G protein coupled receptors, toll-like receptors, growth factor receptors) is responsible for differences in SIL sensitivity between different NSCLC cell lines, see Fig. 7B.