IL-6 and IL-22, as inflammatory factors, do not have antiviral activity per se, but can act on target cells through JAK-STAT signaling, which leads to the secretion of interferon-stimulated genes (ISGs) such as antimicrobial peptides (AMPs), serum amyloid A (SAA), beta-defensins (BDs), S100, etc. and contribute to the inflammatory response to defend against viral infections (52–54). Here, SOAT1 is linked to viral infectious disease.