Crosstalk between NSCLC cells and CAFs reduces sensitivity to targeted therapies, as CAFs show high expression levels of IL-6 and oncostatin-M (OSM), leading to paracrine JAK1/STAT3 activation in NSCLC cells, thus resulting in a switch to the EMT phenotype and protection from targeted drug-induced apoptosis. The gene discussed is IL6; the disease is non-small cell lung carcinoma.