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That spells trouble for mitochondria, which become starved of energy and filled with cellular waste

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GSH deficiency compromised the activation of mammalian target of rapamycin-1 (mTOR) and expression of NFAT [nuclear factor of activated T cells] and Myc transcription factors, abrogating the energy utilization and Myc-dependent metabolic reprogramming that allows activated T cells to switch to glycolysis and glutaminolysis. Essentially, the researchers found that in the experimental mice, the control of viruses is impairedmice that lack the Gclc gene have an immunodeficiency