In fact, upon SeV infection, we recently documented the presence of the “inactive” GSK-3 phosphorylated form of β-catenin within the IFIT1 promoter in association with the IRF3 holocomplex in primary, immortalized, and transformed cell lines [74], arguing that the phosphotransferase activity of GSK-3 is required for an optimal type I IFN antiviral response. This evidence concerns the gene IRF3 and infection.