Strategies aimed at mitigating high sBCMA levels and high disease burden as mechanisms of resistance include the development of bispecific antibodies that bind with higher affinity to full length BCMA rather than sBCMA, higher bispecific antibody dose concentrations, combining anti-BCMA bispecific with gamma-secretase inhibitors to increase the density of BCMA molecules on MM cells (and decrease sBCMA), and combining bispecific antibodies with other anti-myeloma agents to help debulk high burden disease (19, 82, 85, 86). This evidence concerns the gene TNFRSF17 and plasma cell myeloma.