Our data show that while untreated CAFs from NSCLC secrete no CCL2, CCL3 and CCL4, in vitro treatment with IFNγ and TNFα induces particularly high levels of CCL2 (~ 100 000 pg·mL−1) as well as CCL3 and CCL4, which could result in recruitment of myeloid cells to the TME. The gene discussed is CCL3; the disease is non-small cell lung carcinoma.