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While our recent studies in mice deficient in AGXT demonstrated enhanced steatohepatitis and hepatic fibrosis with significant enrichment of proinflammatory and profibrotic pathways 12,24 , the current RNA sequencing findings reveal that proinflammatory (chemokine signalling, cytokinecytokine receptor interaction, NF-B and TNF signalling) and profibrotic (focal adhesion signalling, regulation of actin cytoskeleton and ECMreceptor interactions) pathways are significantly suppressed in livers from mice overexpressing AGXT in hepatocytes during MASH

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