Given a previous report indicating that the better response of genotype B than that of genotype C infections in IFN-α therapy was attributed to a higher level of HBeAg seroconversion via IFN-α mediated preC mutations (44), rt269I vs. rt269L, more related to lower HBV replication or the HBsAg level and more related to HBeAg negative serostatus was expected to lead to enhanced IFN-I production. The gene discussed is IFNA1; the disease is infection.