Considering the consistent reports of suppressed AGXT in MASH12,15–17, recent evidence linking AGXT dysfunction and primary hyperoxaluria with liver disease12,15,20,21, the known deleterious effects of oxalate in renal and cardiovascular diseases22–26, together with the rising prevalence of MASH and limited therapy available1,6,7, 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. This evidence concerns the gene AGXT and metabolic dysfunction-associated steatohepatitis.