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 leukemia.