Mouse BAFF (B cell–Activating Factor), also known as BLyS or TNFSF13B, is a member of the tumor necrosis factor (TNF) superfamily and is a key regulator of B cell development, survival, and humoral immunity in mice (Mus musculus). BAFF is produced primarily by monocytes, macrophages, dendritic cells, neutrophils, and stromal cells, and it signals through the receptors BAFF-R (TNFRSF13C), TACI (TNFRSF13B), and BCMA (TNFRSF17) to promote peripheral B cell maturation, immunoglobulin class switching, and maintenance of long-lived plasma cells. In mice, BAFF is essential for transitional B cell survival and follicular B cell homeostasis; BAFF-deficient mice exhibit reduced peripheral B cell numbers, while BAFF overexpression leads to B cell hyperplasia and autoimmunity. Dysregulated BAFF signaling has been implicated in mouse models of systemic lupus erythematosus (SLE), rheumatoid arthritis, multiple sclerosis, and other antibody-mediated autoimmune diseases. In biomedical research, mouse BAFF is widely studied in models of autoimmunity, chronic inflammation, transplant rejection, vaccine responses, and B cell malignancies, where it serves as a critical mediator of B cell–driven immune regulation and a therapeutic target for modulating pathological antibody production.