Canine 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 dogs (Canis lupus familiaris), TWEAK is produced primarily by immune cells such as macrophages, monocytes, 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 canine physiology, the TWEAK–Fn14 signaling axis is involved in inflammatory responses, tissue repair, and regulation of immune cell activity, particularly during tissue injury or infection. Dysregulation of this pathway may contribute to chronic inflammation, tissue remodeling, and cancer-associated processes. Because TWEAK signaling plays important roles in inflammation, immune regulation, and tissue regeneration, canine TWEAK is of interest in veterinary immunology, inflammatory disease research, and oncology, helping to improve understanding of cytokine-mediated signaling and tissue repair mechanisms in dogs.