Intriguingly, a previous study showed that LAP was enhanced in circulating monocytes from patients with hepatic cirrhosis and in a mouse model of liver fibrosis and that LAP inhibition led to increased hepatic inflammation and fibrosis, suggesting that LAP could act as a compensatory mechanism preventing MDMs reprogramming toward a proinflammatory phenotype (41). This evidence concerns the gene TGFB1 and Hepatic fibrosis.