In these models, HCC development is driven by selective repopulation of Fah-positive hepatocytes expressing the transfected genes and by the cytotoxic microenvironment of Fah mutant livers.[97], [98], [99] Sequential phenotypic changes in diseased liver, such as the emergence of dysplastic foci, nodules, and HCC further support oncogenic transformation of mature hepatocytes.100. This evidence concerns the gene FAH and hepatocellular carcinoma.