Serum CXCL10 levels are elevated in NASH patients while CXCR3 deficiency or deletion of CXCL10 limits liver inflammation, injury and fibrosis (57), and thus the pathogenesis of NASH is reduced in mice (58).Therefore, the effect of IFN-γ deficiency on NASH is partially attributed to the suppressed CXCL10-CXCR3 signaling (Figure 1). This evidence concerns the gene CXCR3 and metabolic dysfunction-associated steatohepatitis.