Moreover, human gene expression data analysis revealed that TSC22D3 mRNA expression is downregulated in NAFLD patients with LF and correlates inversely with that of CCL2. Therefore, our data show that GILZ restrains LF development by controlling CCL2-dependent leukocyte trafficking into the liver, and that this pathway can be targeted therapeutically to restrain LF development and/or progression. Here, TSC22D3 is linked to metabolic dysfunction-associated steatotic liver disease.