As neutrophil accumulation into areas characterized by molecular and microenvironmental structural anomaly is a function mainly of the balance of CXCR2 and CXCR4 ligands and the neutrophil cell surface ratio of CXCR2:CXCR4 chemokine receptors (76), modulation of signaling via these receptors was proposed to be potentially therapeutic for T2D progression, IR, and possibly NAFLD. This evidence concerns the gene CXCR4 and metabolic dysfunction-associated steatotic liver disease.