β-Catenin deletion in SB-HDTVi induced Akt-NRas HCC in β-catenin floxed mice through simultaneous administration of pCMV-cre or control led to a significant improvement in overall survival and less tumor burden in pCMV-Cre compared to control, although tumors still persisted (Supplementary Fig. 4i). The gene discussed is AKT1; the disease is hepatocellular carcinoma.