Most recently, it has been shown that stimulation with CCL18 activated STAT3 signaling pathway in oral cancer cells [18]. In the present study, we showed that DHA treatment dramatically decreased p-STAT3 levels, the activated form of STAT3, in NSCLC cells, which was remarkably rescued by exogenous CCL18, thereby suggesting that DHA inhibits EMT and metastasis possibly by interfering with CCL18/STAT3 signaling pathway in NSCLC cells. This evidence concerns the gene CCL18 and lip and oral cavity carcinoma.