Moreover, targeting a certain lipid metabolism pathway would be a potential therapeutic way to chronic hepatitis B. Given that many studies are limited to cells and animal models and evidence is far from conclusive, more well-designed clinical studies are needed to elucidate the mechanism of this interaction and to discover metabolic targets that could suppress HBV replication or improve the anti-HBV effect of IFN or nucleot(s)ide analogs. The gene discussed is IFNA1; the disease is chronic hepatitis B virus infection.