Mouse TWEAK (TNF-like Weak Inducer of Apoptosis, also known as TNFSF12) is a cytokine belonging to the tumor necrosis factor (TNF) superfamily, which includes related ligands such as TNF-α, Fas ligand (FasL), CD40 ligand (CD40L), TRAIL, and RANKL that regulate immune signaling, apoptosis, and tissue remodeling. In mice (Mus musculus), TWEAK is produced primarily by immune cells such as macrophages, monocytes, dendritic cells, and T lymphocytes, and can also be expressed by endothelial cells and other tissue cells during inflammation or tissue injury. TWEAK exerts its biological effects mainly through binding to its receptor Fn14 (fibroblast growth factor–inducible 14, TNFRSF12A), activating intracellular signaling pathways including NF-κB, MAPK, and other inflammatory signaling cascades that regulate cell survival, proliferation, apoptosis, and cytokine production. In mice, the TWEAK–Fn14 signaling axis has been extensively studied in models of tissue injury, inflammatory disease, and cancer, where it contributes to immune cell activation, tissue remodeling, angiogenesis, and regeneration. Murine studies have also shown that TWEAK signaling plays important roles in muscle regeneration, kidney injury, liver inflammation, and autoimmune disease models, highlighting its involvement in both inflammatory pathology and tissue repair mechanisms. Because mice are widely used as experimental models in immunology and disease research, characterization of mouse TWEAK has been critical for understanding TNF superfamily signaling pathways and their roles in inflammation, tissue damage, and regenerative responses.