Since the JAK–STAT pathway is considered to be a central player in inflammation-mediated tumorigenesis, the implication of JAK–STAT signaling and the therapeutic potential of JAK1/2 inhibition was investigated in K-RAS-driven lung adenocarcinoma, and data showed that JAK1 and JAK2 are activated in human lung adenocarcinoma and that increased activation of JAK–STAT signaling correlated with disease progression and K-RAS activity in human lung adenocarcinoma [20]. Here, KRAS is linked to lung adenocarcinoma.