Tnfrsf17, also known as B-cell maturation antigen (BCMA), is a transmembrane glycoprotein in the tumor necrosis factor receptor superfamily. It is preferentially expressed by mature B lymphocytes, and its overexpression and activation are associated with multiple myeloma (MM) [1]. BCMA plays a role in cell-cell signaling and regulation of B-cell function.

In some MM patients treated with anti-BCMA chimeric antigen receptor T cell (CAR T) or bispecific T cell engager (TCE) therapies, MM relapse was driven by BCMA-negative clones harboring focal biallelic deletions at the Tnfrsf17 locus at relapse or by selective expansion of pre-existing subclones with biallelic Tnfrsf17 loss [2]. This indicates that Tnfrsf17 loss can lead to antigen escape and treatment resistance in MM.

In conclusion, Tnfrsf17, or BCMA, is a key molecule in B-cell function and is of great significance in MM. Gene knockout-related events in Tnfrsf17 can lead to antigen escape in MM patients receiving anti-BCMA therapies, highlighting the importance of understanding Tnfrsf17's role for better treatment strategies in MM.