To further explore the molecular mechanisms underlying the involvement of NAC1-mediated LDHA expression in HBV immune escape, liver cirrhosis, and HCC development, we treated HBV transgenic mice induced by CD137 monoclonal antibodies with NAC1 silencing, or simultaneous NAC1 silencing and overexpression of LDHA. This evidence concerns the gene TNFRSF9 and cirrhosis of liver.