As we know, NF‐κB is considered to be a central mediator of immune and inflammatory response, and IL‐6 could increase the activation of NF‐κB signalling pathway.31, 32, 33 In addition, Wang et al32 demonstrated that IL‐6‐induced intercellular adhesion molecule expression required NF‐κB activation, while our previous study showed that TIM‐4, acting as an adhesion molecule, bound to integrin to promote lung cancer growth.10 As expected, our study found that IL‐6 promoted TIM‐4 expression in NSCLC cell lines via NF‐κB pathway. This evidence concerns the gene NFKB1 and lung cancer.