Initial probing into the mechanism behind the potential tumor suppressive function of IQGAP2 in liver revealed that Iqgap2−/− HCC tumors were characterized by an 8-fold increase in cyclin D1 protein levels (a β-catenin nuclear target), β-catenin translocation from the cellular membrane, accumulation of its dephosphorylated (active) form and loss of membrane E-cadherin expression [5]. This evidence concerns the gene CCND1 and hepatocellular carcinoma.