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If the cell cannot recycle GSSG back into GSH fast enough using an enzyme called glutathione reductase, the cell enters a state of toxic oxidative stress, leading to mitochondrial damage and, eventually, programmed cell death (apoptosis)

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Genome-scale metabolic models of hepatocytes have revealed serine deficiency in patients with non-alcoholic fatty liver disease (NAFLD), while the expression levels of SHMT1 and SHMT2 are significantly down-regulated in the livers of non-alcoholic steatohepatitis (NASH) patients, and PSPH, SHMT1, and BCAT1 (branched-chain amino acid transaminase 1) have been identified as potential therapeutic targets for NASH