The increase in inflammation and fibrosis in the Zrsr1 and Zrsr2 double-deficient livers led to liver damage and the MASH phenotype, which was supported by an increase in ALT and AST levels and hydroxyproline deposits in the livers of these mice (Figure 3, G and H). This evidence concerns the gene ZRSR2 and metabolic dysfunction-associated steatohepatitis.