In non-small cell lung cancer (NSCLC), secretion of oncostatin-M (OSM), a member of the IL-6 cytokine family, by cancer-associated fibroblasts increases STAT3 activity through activation of JAK1 and is a possible mechanism of resistance to targeted therapy such as EGFR and MEK inhibitors[50]. This evidence concerns the gene STAT3 and non-small cell lung carcinoma.