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. The gene discussed is SLC16A3; the disease is Miyoshi myopathy.