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A mechanism for the unchanged tissue glutathione content in riboflavin deficiency could be the increased biosynthesis of glutathione from its precursor amino acids as a compensatory action ( Reference Kaplowitz, Aw and Ookhtens 30 )
CRISPR-based functional genomic screens have uncovered synthetic lethal interactions involving epigenetic regulators such as KDM5A, EZH2, and SMARCA2 in resistant tumor cells, which can be therapeutically exploited with selective inhibitors
New England Journal of Medicine, 385(6), 503-515
Orskov C, and Poulsen SS
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