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The source of WS is the Werner (WRN) DNA helicase gene, which regulates the transcription of the essential NAD+ biosynthetic enzyme Nicotinamide Nucleotide Adenylyltransferase 1 (24,25). NAD+ depletion through disruption of mitochondrial homeostasis is a substantial contributor to the metabolic dysfunction in WS, according to a 2019 study (25)

SAG S-acetyl-glutathione SAG S-acetyl-glutathione a delayed release delivery system designed to protect the molecule from degradation by gastric acids in the stomach and carry the SAG to the small intestine where it can be readily taken up intact by chylomicrons in the gut

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Another study showed that polymorphisms in the proteasome pathway (required for trimming peptides for presentation on MHC) are associated with SJS/TEN [26, 48]