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Considering the consistent reports of suppressed AGXT in MASH 12,15,16,17 , recent evidence linking AGXT dysfunction and primary hyperoxaluria with liver disease 12,15,20,21 , the known deleterious effects of oxalate in renal and cardiovascular diseases 22,23,24,25,26 , together with the rising prevalence of MASH and limited therapy available 1,6,7 , there is a strong rationale to better understand impaired oxalate metabolism in MASH and to evaluate the therapeutic potential of targeting this dysregulated metabolic pathway