Furthermore, increased hepatic expression of interferon regulatory factor (IRF)3 and IRF7, which are key transcription factors of type I IFNs, as well as increased hepatic expression of several interferon-stimulated genes (ISGs), which are target genes for type I IFNs, were also observed in NAFLD, implying that hepatic steatosis possibly induces the local production of IFN-α and IFN-β in the liver of NAFLD mice compared to WT mice, thus contributing to metabolic dysregulation [118]. Here, IFNA1 is linked to metabolic dysfunction-associated steatotic liver disease.