In the current study, we have demonstrated that B56γ was upregulated and positively correlated with HBx expression in the specimens of liver diseases’ patients, HBV-infected primary human hepatocytes (PHHs) in human-liver-chimeric (HLC) mice, HBx-transgenic (Tg) mice, HBV-infected HepG2 cells expressing sodium taurocholate cotransporting polypeptide (NTCP), and several HBx-expressing hepatic cells. This evidence concerns the gene SLC10A1 and liver disorder.