This review article discusses the signaling pathways of IL-6-type cytokines through the gp130/Jak/STAT pathway. These cytokines, including IL-6, IL-11, LIF, OSM, CNTF, and CT-1, play a crucial role in regulating complex cellular processes such as gene activation, proliferation, and differentiation. The signaling process begins with ligand-induced receptor dimerization, leading to the activation of Janus kinases (Jaks) and the recruitment and phosphorylation of STAT family transcription factors. These factors dimerize, translocate to the nucleus, and bind to enhancer elements of target genes, leading to transcriptional activation. The key players in this signaling pathway include cytokines, receptor components, Jaks (Jak1, Jak2, Tyk2), STATs (STAT1, STAT3), and the tyrosine phosphatase SHP2. The signaling pathway is complex, involving multiple steps such as receptor complex assembly, kinase activation, and transcription factor recruitment. The termination of the signaling pathway involves mechanisms such as tyrosine phosphatases, proteasome, SOCS, PIAS, and receptor internalization via gp130. The IL-6-type cytokines are characterized by their structural similarities, including a four-α-helix bundle, and their shared use of the gp130 receptor subunit for signal transduction. Despite these similarities, they elicit distinct biological responses, as shown by the different phenotypes of knock-out animals. The signaling pathways of these cytokines are highly regulated, with various mechanisms ensuring proper signal transduction and termination. The review also discusses the structural properties of the cytokines and their receptors, the physiological responses they elicit, and the molecular mechanisms involved in their signal transduction via the Jak/STAT pathway. The role of SHP2 in signaling is also discussed, highlighting its involvement in various signal transduction pathways and its interaction with Jaks and Grb2. The review concludes with a discussion on the negative regulation of the gp130/Jak/STAT pathway, including mechanisms such as dephosphorylation and proteolytic degradation.This review article discusses the signaling pathways of IL-6-type cytokines through the gp130/Jak/STAT pathway. These cytokines, including IL-6, IL-11, LIF, OSM, CNTF, and CT-1, play a crucial role in regulating complex cellular processes such as gene activation, proliferation, and differentiation. The signaling process begins with ligand-induced receptor dimerization, leading to the activation of Janus kinases (Jaks) and the recruitment and phosphorylation of STAT family transcription factors. These factors dimerize, translocate to the nucleus, and bind to enhancer elements of target genes, leading to transcriptional activation. The key players in this signaling pathway include cytokines, receptor components, Jaks (Jak1, Jak2, Tyk2), STATs (STAT1, STAT3), and the tyrosine phosphatase SHP2. The signaling pathway is complex, involving multiple steps such as receptor complex assembly, kinase activation, and transcription factor recruitment. The termination of the signaling pathway involves mechanisms such as tyrosine phosphatases, proteasome, SOCS, PIAS, and receptor internalization via gp130. The IL-6-type cytokines are characterized by their structural similarities, including a four-α-helix bundle, and their shared use of the gp130 receptor subunit for signal transduction. Despite these similarities, they elicit distinct biological responses, as shown by the different phenotypes of knock-out animals. The signaling pathways of these cytokines are highly regulated, with various mechanisms ensuring proper signal transduction and termination. The review also discusses the structural properties of the cytokines and their receptors, the physiological responses they elicit, and the molecular mechanisms involved in their signal transduction via the Jak/STAT pathway. The role of SHP2 in signaling is also discussed, highlighting its involvement in various signal transduction pathways and its interaction with Jaks and Grb2. The review concludes with a discussion on the negative regulation of the gp130/Jak/STAT pathway, including mechanisms such as dephosphorylation and proteolytic degradation.