For example, pharmacological inhibition of CCR2+ monocyte recruitment efficiently ameliorates hepatic inflammation and fibrosis in patients with metabolic steatohepatitis.34 S100A4 derived from macrophages in the liver promotes liver fibrosis through hepatic stellate cell activation.35 Pathway analysis further revealed that Cx3cr1+Ccr2+ Mo-macs were enriched for inflammatory pathways and inflammation-activated key genes (Fig. 5c, d). The gene discussed is CX3CR1; the disease is Hepatic fibrosis.