Notably, lowering hepatic oxalate in MASH by genetic (hepatocyte-specific AGXT overexpression by AAV8-AGXT) and pharmacological (GO and LDHA inhibition by MDMG-935P) targeting of oxalate overproduction ameliorates hepatic steatosis, inflammation and fibrosis through induction of PPARα-driven FAO and suppression of monocyte chemotaxis, NF-κB and TGFβ targets (Fig. 8m). Here, TGFB1 is linked to fatty liver disease.