Subsequently, Zhou et al. used flow cytometry to identify macrophages and found that FABP4 in liver sinusoidal endothelial cells may play a pathogenic role in the course of MASLD by activating NF-κB/p65 signaling to promote CXCL10-mediated macrophage M1 polarization and CXCR3 macrophage infiltration [37]. This evidence concerns the gene CXCR3 and metabolic dysfunction-associated steatotic liver disease.