The TNFSF13B gene encodes B cell-activating factor (BAFF), a critical cytokine for B cell survival and maturation, primarily expressed by monocytes, macrophages, dendritic cells, and T cells ^[1]. BAFF, a member of the tumour necrosis factor (TNF) superfamily, functions through binding to receptors on B cells, including BAFF-R, TACI, and BCMA. Activation of these receptors initiates the NF-κB and MAPK signaling cascades, leading to B cell survival, proliferation, and immunoglobulin production ^[1-2]. This cytokine is essential for humoral immunity and the development of lymphoid tissues ^[1]. Aberrant BAFF expression and signaling are implicated in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis. BAFF overexpression can drive B cell hyperactivity and the production of autoantibodies, contributing to these conditions ^[2-3]. Clinically, monoclonal antibodies targeting BAFF, such as belimumab, are employed in the treatment of SLE ^[4]. In the tumor microenvironment, BAFF exhibits a complex role, supporting B cell lymphomas and influencing the immune response to solid tumours, exhibiting context-dependent pro- and anti-tumourigenic effects ^[5]. This multifaceted role highlights BAFF as a key therapeutic target in autoimmune diseases and specific B cell malignancies ^[1-5].

The B6-hBAFF(TNFSF13B) mouse is a humanized model generated using gene editing technology, in which the protein-coding sequence (CDS) encoding the extracellular domain of the human TNFSF13B protein is integrated into a specific site within the mouse Tnfsf13b gene, while retaining the endogenous gene sequence encoding the mouse cytoplasmic and transmembrane domains. Homozygous B6-hBAFF(TNFSF13B) mice are viable and fertile. This model can be used to study the pathological mechanisms and therapeutic approaches of autoimmune diseases and specific B cell malignancies, as well as for the development of BAFF-targeted drugs.