In different phases of lung cancer development and its therapeutic management, IL6 drives multiple molecular mechanisms responsible for the epithelial-mesenchymal transition (EMT) (98, 99) and therapy resistance, such as infiltration of pro-tumor macrophages after irradiation through the upregulation of CCL2/CCL5 in vitro human and in vivo mouse lung tumor models (100). This evidence concerns the gene IL6 and neoplasm.