Our data indicate that CXCL10 genetic deletion conveys several salutary effects that are principally mediated by diminished hepatic macrophage trafficking to the liver, infiltration and activation with subsequent decrease in hepatic injury and fibrosis; furthermore, we substantiate our findings and demonstrate that genetic deletion of the CXCL10 cognate receptor CXCR3 reduces diet-induced murine NASH. This evidence concerns the gene CXCR3 and metabolic dysfunction-associated steatohepatitis.