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Thus, by silencing CDO1, NRF2-addicted cancer cells maintain a large intracellular pool of cysteine for the glutathione synthesis, resulting from the increased cysteine uptake by xCT and decreased cysteine decomposition

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Restoring DLX-mediated GABAergic neuron differentiation or enhancing GABA signaling (e.g., via GABAA receptor agonists) could potentially rescue circuit imbalances in DLX-related ASD subtypes