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[7] There is compelling evidence that some ME/CFS patients are low in methylation cycle metabolites, and there are some studies that provide direct evidence of methylation cycle dysregulation in ME/CFS

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In mice, the acute systemic inhibition of GSH synthesis by L-buthionine-S-R-sulfoximine (BSO) triggers a protective response and a subsequent increase in the CNS GSH content

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They found that FOXO4 helps keep senescent Leydig cells alive and prevents them from undergoing programmed cell death (apoptosis)

As newer checkpoint inhibitors emerge, the role of ipi3 remains to be further defined