Collectively, the above findings suggested that NF-κB-tailored proteasome inhibition in the mouse model of adenocarcinoma-induced MPE suppresses the gene expression of NF-κB-dependent mediators in pleural LLC tumors, which are required for the paracrine promotion of inflammation, vascular leakiness, and angiogenesis, the major known pathways for MPE induction by cancer cells. The gene discussed is NFKB1; the disease is adenocarcinoma.