Additionally, Smad7 activity in other hepatic cell populations, such as hepatocytes and stellate cells/myofibroblasts, may have a larger impact on liver fibrosis, when lacking Smad7, as it is reported that global and hepatocyte-specific, Smad7-deficient mice have pronounced aberrant phenotypes in diverse liver disease models, such as CCl4- and alcohol-induced liver injury and hepatocellular carcinoma [14,15,20,21]. This evidence concerns the gene SMAD7 and hepatocellular carcinoma.