While our recent studies in mice deficient in AGXT demonstrated enhanced steatohepatitis and hepatic fibrosis with significant enrichment of proinflammatory and profibrotic pathways12,24, the current RNA sequencing findings reveal that proinflammatory (chemokine signalling, cytokine–cytokine receptor interaction, NF-κB and TNF signalling) and profibrotic (focal adhesion signalling, regulation of actin cytoskeleton and ECM–receptor interactions) pathways are significantly suppressed in livers from mice overexpressing AGXT in hepatocytes during MASH. The gene discussed is AGXT; the disease is Hepatic fibrosis.