One hypothesis for the inferior DOR and PFS outcomes seen in the prior BCMA-TT cohort is that the prior anti-BCMA therapy may have contributed to a greater rate of development of myeloma subclones with monoallelic or biallelic BCMA loss that then experienced clonal expansion amidst the therapeutic pressure of ide-cel treatment. This evidence concerns the gene TNFRSF17 and plasma cell myeloma.