Xu et al. found that while activating BMI1 or RasV12 alone was insufficient to enhance HCC development, over-expression of these two genes at the same time is suspected to promote tumor formation in mice [231].This results suggested that BMI1 can cooperate with other oncogenes to stimulate hepatocarcinogenesis in vitro and in vivo. This evidence concerns the gene BMI1 and hepatocellular carcinoma.