On the other hand, direct determination of cell death also confirmed that OTULIN-KO MDA-MB-231 cells reconstituted with either the Y56F or K64/66R mutant OTULIN both resulted in increased cancer cell survival under genotoxic stress via dysregulated NF-κB signaling since these effects were abolished by overexpressing an IκBα superrepressor (IκBα SR) (43) or cotreatment with an IKKβ inhibitor TPCA-1 (SI Appendix, Fig. S5). Here, IKBKB is linked to cancer.