Similarly, could approaches of increasing mitochondrial mass (such as overexpression of PGC1α, which is beneficial in inflammatory demyelination and regulates Idh3a expression as part of its broad transcriptional effects11,52) be synergistic with targeting the TCA cycle to unblock energy provision in axons and resolve their dystrophy in conditions like MS? The gene discussed is IDH3A; the disease is myeloid sarcoma.