EGFR tyrosine kinase inhibitors (TKIs), such as afatinib and dacomitinib, could activate STAT3 via autocrine interleukin-6 (IL-6) production, and that blockade of the IL-6R/JAK1/STAT3 signaling pathway potentiated sensitivity to those EGFR TKIs in NSCLC cells (Kim et al., 2012). The gene discussed is STAT3; the disease is non-small cell lung carcinoma.