Interestingly, erlotinib, as an RTK inhibitor, increases STAT3 phosphorylation (Tyr705) in EGFR-mutant ono-small-cell lung cancer (NSCLC) cells through an autocrine loop, whereas knockdown of STAT3 decreases erlotinib-resistant colony numbers in the presence of erlotinib. This evidence concerns the gene STAT3 and small cell lung carcinoma.