To assess the importance of LUBAC and NF-κB activity in the chemotherapy resistance of LSCC, we treated primary KF LSCC tumor cells with gliotoxin, which inhibits LUBAC by direct binding to HOIP (Sakamoto et al., 2015), or with a TAK1 inhibitor, 5Z-7-oxozeaenol (5Z-7), which is required for activation of IKK and IKK-mediated degradation of IκB (Wang et al., 2001). This evidence concerns the gene MAP3K7 and neoplasm.