Despite the high dependence of multiple myeloma (MM) cells on glutamine—driven by elevated c-Myc expression—and the established link between increased glutamine utilization and MM pathogenesis, the absence of a compensatory rise in glutamine anaplerosis into the TCA cycle following a reduction in extracellular lactate anaplerosis through dual MCT1 and MCT4 blockade remains unresolved. Here, SLC16A3 is linked to plasma cell myeloma.