Mouse Leukemia Inhibitory Factor (LIF) is a multifunctional cytokine belonging to the IL-6 family—which includes IL-6, IL-11, oncostatin M (OSM), ciliary neurotrophic factor (CNTF), cardiotrophin-1 (CT-1), cardiotrophin-like cytokine factor 1 (CLCF1), and IL-27—and signals through receptor complexes containing the shared gp130 subunit. In mice (Mus musculus), LIF binds to the LIF receptor (LIFR) in association with gp130, activating JAK/STAT3, MAPK, and PI3K signaling pathways that regulate cell survival, differentiation, immune modulation, and tissue repair. Murine LIF is best known for its essential role in maintaining pluripotency of embryonic stem cells in vitro via STAT3 activation and for its requirement in embryo implantation and uterine receptivity in vivo. Beyond reproductive and developmental biology, mouse LIF is involved in hematopoiesis, neural regeneration, and modulation of inflammatory responses in models of colitis, lung injury, neuroinflammation, fibrosis, and cancer. Dysregulated LIF/STAT3 signaling has been linked to tumor progression and stromal remodeling in murine cancer models. Because mice are the primary genetic model organism for biomedical research, characterization of LIF has been instrumental in defining IL-6 family signaling mechanisms, stem cell biology, cytokine-driven inflammation, and development of STAT3-targeted therapeutic strategies relevant to human disease.