In fact, the results from non-liver derived cell lines and HBV replication mouse model (with/without HNF4α inhibition) had confirmed that HNF4α supported high replication level of TA mutation, [20] which may contribute to the aggravation of hepatitis B. Considering the positive correlation between HNF4α expression and HBV replication in liver tissue of IHBV infections, and avoiding the interference of HBV DNA level on HNF4α expression, only patients with serum HBV DNA less than 5 log10 copies/mL were included, and the mean level of HBV DNA was comparable between each group in this study. This evidence concerns the gene HNF4A and hepatitis B virus infection.