Therefore, to evaluate whether ChREBP was indeed required during HCC development, in cancer cells harboring alterations in these key identified drivers of human hepatocarcinogenesis, we stably overexpressed TERT, cmyc, jarid1b or stably inhibited p53, axin1 or Arid1a in the liver of either wild type (WT) or liver-specific ChREBP knockout mice (KO), using the sleeping beauty (SB) transposon system and the CRISPR/Cas9 approaches (Fig. 9c, d). This evidence concerns the gene MLXIPL and hepatocellular carcinoma.