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Under physiological conditions, more than 98% of the total GSH pool exists in the reduced form, thereby shaping cellular redox potential and influencing proliferation, differentiation, and cell death 5 .Although the GSH/GSSG ratio has long been regarded as an indicator of cellular redox status, recent live-cell studies using genetically encoded redox sensors indicate that increases in GSSG are typically transient and compartmentalized rather than sustained intracellular accumulations 6,7

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In a disorder defined by symptoms related to fatigue, autonomic nervous system problems [e.g., (46)], and putative neuroimmune signaling [e.g., (47) reported brainstem hypoperfusion in ME/CFS patients vs

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