The tumor microenvironment in HBV-related HCC is significantly influenced by these virus–host interactions, with APOBEC3B contributing to the induction of HBx mutations that can overexpress PLA2R (phospholipase A2 receptor), activate the NLRP3 inflammasome in hepatocytes, and lead to the generation of reactive oxygen species (ROS) and accelerated inflammatory responses. This evidence concerns the gene APOBEC3B and neoplasm.