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Gliotoxin biosynthesis may be curtailed in order to diminish GSH incorporation into the gliotoxin biosynthetic pathway, thereby allowing for an increase in intracellular GSH

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1,4 Hyperglycemia, dyslipidemia, and insulin resistance activate various metabolic pathways, resulting in oxidative stress, mitochondrial dysfunction, inflammation, and microvascular damage, culminating in neuronal injury, Schwann cell damage, and myelin sheath degeneration

Specifically, FOXO4-DRI peptide has been researched as a decoy that may compete with FOXO4 for p53 binding, so it may disrupt the FOXO4p53 interaction in laboratory systems