The TNFRSF17 gene, also known as BCMA, encodes a protein belonging to the tumor necrosis factor receptor superfamily. This protein is predominantly expressed in mature B lymphocytes, particularly plasma cells, with lower expression in early B cells and non-B cells ^[1-2]. As a type III transmembrane glycoprotein, TNFRSF17 plays a critical role in B cell survival and differentiation, acting as a key regulator of B cell maturation ^[2]. Functionally, TNFRSF17 primarily acts as a receptor for the B cell-activating factor (BAFF). Upon BAFF binding, it activates both the classical NF-κB pathway and the non-classical MAPK8/JNK pathway, subsequently regulating downstream gene expression to promote B cell survival, proliferation, and antibody secretion. Furthermore, TNFRSF17 can interact with TNFR-associated factors (TRAFs) 1, 2, and 3, further mediating physiological processes related to cell differentiation and growth ^[1-2]. Multiple studies have demonstrated that the TNFRSF17 gene and its protein are associated with various B cell-related diseases. Notably, this gene exhibits abnormally high expression in diseases such as multiple myeloma and systemic lupus erythematosus, rendering it a potential therapeutic target for these conditions ^[3-4].

The B6-hBCMA (TNFRSF17) mouse is a humanized model constructed using gene editing technology, where the mouse BCMA endogenous extracellular domain was replaced with the human BCMA extracellular domain. Homozygous B6-hBCMA (TNFRSF17) mice are viable and fertile. This model can be used for studying the pathological mechanisms and therapeutic approaches of multiple myeloma, systemic lupus erythematosus, and various B cell-related diseases and for the development of BCMA-targeted drugs.