Its function remained obscure until a recent study using human liver cell line HuH7 cells revealed that the level of EGOT was dramatically induced by viral infection, such as HCV, influenza, and Semliki Forest virus (SFV), and high doses of IFNα stimulation (58), and furthermore, knockdown experiment in HCV infected cells revealed that EGOT negatively regulated antiviral responses through inhibiting a subset of ISGs' expression as a negative feedback regulatory mechanism of IFN pathway. The gene discussed is IFNA2; the disease is viral infectious disease.