As a result, glycolysis inhibition, ihTh17 cell-specific ablation of IFNγ, or modulation of CXCR3-CXCL9/10 axis conferred protection against hepatocellular damage and hepatic accumulation of ihTh17 cells in murine models of NASH (75). This evidence concerns the gene IFNG and metabolic dysfunction-associated steatohepatitis.