Regulation by macroH2A1 of oncogenes and/or tumor suppressors’ expression in hepatocytes could be particularly relevant for fatty liver-associated HCC, since the activities of these genes often link mechanistically hepatic steatosis to the onset of HCC, as we have previously shown for tumor suppressor phosphatase with tensin homology (PTEN) [23], [24], [25]. This evidence concerns the gene PTEN and steatosis.