Both inhibitors selectively block their respective targets within the JAK-STAT signaling pathway, which is essential for mediating immune responses against viral infections (38, 39), and JAK-1 antagonist (420099) primarily inhibits JAK-1 phosphorylation, disrupting the downstream signaling cascade initiated by cytokines like type I and II interferons, leading to a broad suppression of immune responses and a reduction in COX-2 and PGE2 levels in IBV-infected tracheal explants (40). This evidence concerns the gene SOAT1 and viral infectious disease.