Mouse 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 mice (Mus musculus), RANKL is expressed primarily by osteoblasts, bone marrow stromal cells, activated T lymphocytes, and other immune cells, where it plays a key role in bone remodeling and immune system regulation. RANKL binds 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 interaction with RANK, thereby maintaining balanced bone turnover. In mice, the RANKL–RANK–OPG signaling axis has been extensively studied using genetic knockout and transgenic models, which have demonstrated that disruption of RANKL signaling results in severe osteopetrosis, absence of osteoclasts, and defects in lymph node development. Mouse RANKL also plays important roles in immune regulation and mammary gland development during pregnancy. Because mice are widely used as experimental models for bone biology, immunology, and cancer research, characterization of mouse RANKL has been critical for understanding osteoclast regulation, skeletal development, and immune signaling pathways, providing insights relevant to human bone diseases and therapeutic development.