With regard to HCC, we have so far demonstrated that ubiquitous genetic inactivation of Ccne1 or hepatocyte-specific deletion of its interacting kinase subunit Cdk2 inhibited HCC initiation [10], while interventional depletion of Ccne1, but not of Cdk2, in hematopoietic cells, hepatocytes and lymphocytes ameliorated the progression of HCC [20]. This evidence concerns the gene CDK2 and hepatocellular carcinoma.