The original aim of our experiments was to address the role of IKK2-mediated NF-κB activation in hepatocytes in HCC development in Mdr2−/− mice, prompted by the study of Pikarsky et al. [7] who showed that NF-κB inhibition in hepatocytes by expression of an IκBα super-repressor could prevent or delay HCC development in Mdr2-deficient mice. Here, NFKB1 is linked to hepatocellular carcinoma.