Mechanistically, we could demonstrate that damaged EGFR-deficient hepatocytes undergo more necrosis and apoptosis and produce increased levels of IL-1β leading to enhanced stimulation of Kupffer cells, which subsequently produce high levels of IL-6, thus triggering massive compensatory hepatocyte proliferation ultimately leading to increased HCC formation (Figure 2) [76]. This evidence concerns the gene EGFR and hepatocellular carcinoma.