Indeed, K‐RAS‐mutated lung AC cells secrete pro‐inflammatory cytokines including interleukin (IL)‐6 that activate JAK1 and JAK2 via glycoprotein 130 in an autocrine loop, thereby promoting tumor cell survival.7, 10, 11 On the other hand, genetic deletion of STAT3, a key signaling mediator of JAK1/2, enhances K‐RAS‐driven lung tumorigenesis, and activation of the interferon/JAK/STAT axis induces cell apoptosis and suppresses tumorigenesis in various experimental tumor models.12, 13, 14, 15, 16. The gene discussed is JAK2; the disease is neoplasm.