We reasoned that agents targeting a nonredundant, downstream module within this critical survival axis of the NF-κB pathway and having functional restriction to the cancer cells (e.g., the GADD45β/MKK7 module in the case of MM) would provide a more selective and, therefore, more effective therapy, lacking the dose-limiting toxicities of conventional drugs globally targeting NF-κB. The gene discussed is NFKB1; the disease is cancer.