Indeed, accumulating evidence has demonstrated that numerous ISGs can be directly upregulated following virus infection independent of IFN signaling, whereas typical ISGs are driven by JAK-STAT signaling, other virally stimulated genes are upregulated through the IRF3 and NF-κB pathways [36], including OAS and MxA [37], or through the BATF2-IRF1 as a potential antiviral host machinery in the absence of IFN signaling [33]. Here, SOAT1 is linked to viral infectious disease.