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Multiple cellular problems attributed to dysregulation of GSH and GSH-dependent enzymes contributes to impairment in the function of mitochondria, elevation in oxidative damage, disruption of intracellular signal transduction pathways, protein aggregation, and eventually cell death

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In addition, the possibility to manipulate SLC25A39 and/or to regulate the amount of GSH that enters mitochondria also offers the opportunity to study the importance of mitochondrial GSH in more detail, especially in mitochondria-rich tissues like liver or kidney

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The loss of CNTNAP2 leads to synaptic changes in vitro , reduced inhibitory and axonal excitability defects in acute hippocampal slices (102, 103)