Therefore, our observation of an increased development of HCCs in Tax1BP1−/− mice with increased numbers of non-parenchymal liver cells and increased levels of proinflammatory cytokines upon stimulation of macrophages fits in the theory of a tumor promoting effect of NFκB in myeloid derived cells by enhancing anti-apoptotic signaling in hepatocytes triggered by Kupffer and hepatic stellate cells predisposes transformed cells to cancer development3–5. This evidence concerns the gene NFKB1 and neoplasm.