To explore the potential mechanisms through which Q11 is effective in lung cancer, we examined the IL‐6/STAT3 pathway and the MAPK/ERK pathway (p38‐MAPK, ERK1/2), which were proven to play a critical role in tumorigenesis and the inflammatory response.[35, 36, 37] We found that greater levels of IL‐6, phosphorylated STAT3, phosphorylated p38‐MAPK and phosphorylated ERK1/2 were associated with a higher CYP2E1 level in the peritumoral tissue of NSCLC patients (Figure 6A). Here, STAT3 is linked to lung cancer.