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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

In murine models, NNMT knockdown did not induce the accumulation of NAM in livers and adipose tissues, nor did it cause significant alterations in the intracellular levels of NAD + in hepatocytes (Kraus et al., 2014