Switching to alternative antigen targets, such as transitioning from BCMA-directed therapies to GPRC5D- or FcRH5-directed constructs, has demonstrated clinical efficacy in the setting of antigen loss in multiple myeloma and is similarly being explored with CD19- and CD20-directed therapies in B-cell malignancies [132,133]. The gene discussed is TNFRSF17; the disease is plasma cell myeloma.