Studies have shown that the inhibition of IFN-λ signal by SOCS-1 induced by influenza virus leads to an increase in the adaptability of host IFN-λ expression, thereby protecting cells from virus infection, but it leads to the overproduction of IFN-λ, which ultimately results in the sabotage of antiviral response (136). This evidence concerns the gene SOCS1 and viral infectious disease.