Rat RANKL (Receptor Activator of Nuclear Factor κB Ligand, also known as TNFSF11, TRANCE, or OPGL) 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), and TRAIL that regulate immune signaling, apoptosis, and cellular differentiation. In rats (Rattus norvegicus), RANKL is expressed primarily by osteoblasts, bone marrow stromal cells, activated T lymphocytes, and other immune cells, where it plays a central role in bone remodeling and immune system regulation. RANKL functions by binding to its receptor RANK (receptor activator of NF-κB) on osteoclast precursors and mature osteoclasts, activating intracellular signaling pathways including NF-κB, MAPK, and NFATc1, which promote osteoclast differentiation, activation, and bone resorption. The activity of RANKL is tightly regulated by osteoprotegerin (OPG, TNFRSF11B), a soluble decoy receptor that binds RANKL and prevents its interaction with RANK, thereby maintaining balanced bone turnover. In rats, the RANKL–RANK–OPG signaling axis is widely studied in experimental models of osteoporosis, bone fracture healing, arthritis, and bone metastasis, where dysregulated RANKL signaling contributes to increased osteoclast activity and pathological bone loss. Because rats are commonly used in orthopedic, metabolic bone disease, and pharmacological research, characterization of rat RANKL has contributed significantly to understanding osteoclast biology, skeletal remodeling, and therapeutic strategies targeting bone resorption.