The article discusses the mechanisms of type-I and type-II interferon (IFN)-mediated signaling, highlighting the complex interplay of signaling pathways that underlie the diverse biological effects of IFNs. Interferons are cytokines with antiviral, antiproliferative, and immunomodulatory functions, and their signaling is mediated through distinct pathways. The type-I IFN receptor, composed of IFNAR1 and IFNAR2, activates JAK kinases (TYK2 and JAK1), leading to the phosphorylation and activation of STAT proteins, which then translocate to the nucleus to initiate gene transcription. The type-II IFN receptor, composed of IFNGR1 and IFNGR2, activates JAK1 and JAK2, leading to the phosphorylation and activation of STAT1, which also translocates to the nucleus to initiate gene transcription. In addition to the JAK-STAT pathway, other signaling cascades, such as the p38 and PI3K pathways, are also involved in IFN-mediated signaling. The p38 pathway is particularly important in the generation of IFN-mediated signals, and its activation is regulated by upstream effectors such as RAC1 and VAV. The PI3K pathway is also involved in IFN-mediated signaling, and its activation is regulated by IRS proteins and other phosphoproteins. The PI3K pathway can also regulate the serine phosphorylation of STAT1, which is important for full transcriptional activation. The article also discusses the role of other signaling pathways, such as the MAPK and JNK pathways, in IFN-mediated signaling. These pathways are involved in the regulation of various cellular processes, including apoptosis, cell proliferation, and gene transcription. The article concludes that the signaling pathways involved in IFN-mediated signaling are complex and multifaceted, and that a better understanding of these pathways is essential for the development of new therapeutic strategies for the treatment of viral infections and cancer.The article discusses the mechanisms of type-I and type-II interferon (IFN)-mediated signaling, highlighting the complex interplay of signaling pathways that underlie the diverse biological effects of IFNs. Interferons are cytokines with antiviral, antiproliferative, and immunomodulatory functions, and their signaling is mediated through distinct pathways. The type-I IFN receptor, composed of IFNAR1 and IFNAR2, activates JAK kinases (TYK2 and JAK1), leading to the phosphorylation and activation of STAT proteins, which then translocate to the nucleus to initiate gene transcription. The type-II IFN receptor, composed of IFNGR1 and IFNGR2, activates JAK1 and JAK2, leading to the phosphorylation and activation of STAT1, which also translocates to the nucleus to initiate gene transcription. In addition to the JAK-STAT pathway, other signaling cascades, such as the p38 and PI3K pathways, are also involved in IFN-mediated signaling. The p38 pathway is particularly important in the generation of IFN-mediated signals, and its activation is regulated by upstream effectors such as RAC1 and VAV. The PI3K pathway is also involved in IFN-mediated signaling, and its activation is regulated by IRS proteins and other phosphoproteins. The PI3K pathway can also regulate the serine phosphorylation of STAT1, which is important for full transcriptional activation. The article also discusses the role of other signaling pathways, such as the MAPK and JNK pathways, in IFN-mediated signaling. These pathways are involved in the regulation of various cellular processes, including apoptosis, cell proliferation, and gene transcription. The article concludes that the signaling pathways involved in IFN-mediated signaling are complex and multifaceted, and that a better understanding of these pathways is essential for the development of new therapeutic strategies for the treatment of viral infections and cancer.