To determine whether the amplification of an inflammatory program by GSK126 could be therapeutically exploited in NSCLC, we next investigated whether applying GSK126 would enhance responses when cells were subsequently treated with a combination of BTZ plus NM, which target the proteasome-dependent activation of NF-κB, and inflammation induced by Kras and Ezh2 depletion, respectively. This evidence concerns the gene NFKB1 and non-small cell lung carcinoma.