It was reported that TIM‐4 inhibited cytokine production via NF‐κB signalling pathway19 and had no effect on STAT3 phosphorylation,20 while IL‐6 could increase the activation of NF‐κB16 and STAT3 signalling pathway.21 We then tested the changes of these signal molecules in IL‐6‐induced up‐regulation of TIM‐4 in lung cancer cells with NF‐κB inhibitor or STAT3 inhibitor, respectively. This evidence concerns the gene STAT3 and lung cancer.