Canonical activation of the NF-κB pathway depends on degradation of its inhibitor, IκBα, which retains the cytosolic distribution of p65/p50 heterodimer by direct binding with them.1 Hyper activation of NF-κB has been linked to abnormal proliferation, tumor initiation and progression in many types of cancer, including myeloma, leukemia and breast cancer.2 This evidence concerns the gene NFKB1 and plasma cell myeloma.