In the present study, it was shown that the proinflammatory cytokine IL-1β, which is abundantly produced in lung cancer [10], leads to increased TF formation in lung cancer cells via both Src/EGFR/p42/44 MAPK-dependent and EGFR-independent signaling pathways, the latter being mediated via p38 MAPK and JNK (Figure 7). This evidence concerns the gene TF and lung carcinoma.