The EGFR–TKI gefitinib had little effect on the phosphorylation of EGFR or that of AKT, ERK, or STAT3 in EBC-1 or H1993 cells (Figure 1B), whereas it markedly inhibited the phosphorylation of these molecules in EGFR mutation-positive lung cancer cell lines (PC9 and HCC827) that manifest constitutive activation of the EGFR kinase (Figure 1C, data not shown). This evidence concerns the gene STAT3 and lung cancer.