Because the components of the IL6/JAK/STAT3 pathway are aberrantly hyperactivated in various tumors and targeting these components can inhibit tumor growth (Johnson et al., 2018), lung cancer cells in which the levels of SETDB1 are high are probably supposed to have a natural ability to control the IL6/JAK/STAT3 pathway, creating an environment that is unfavorable for tumor growth. Here, STAT3 is linked to lung carcinoma.