In cancer cells, the binding of BDR4 to RelA/NF-κB subunit blocks RelA ubiquitinilation and its subsequent proteasome-mediated degradation, leading to sustained nuclear NF-κB activation and, therefore, showing a mechanisms involved in aberrant cell proliferation (Wu et al., 2013; Zou et al., 2014). This evidence concerns the gene NFKB1 and cancer.