Functional studies showed that ANXA1 attenuated CCl4-induced hepatic fibrosis in mice, and the mechanism may be that ANXA1 targets the N-formylpeptide receptor (FPR) to regulate macrophage function and thus inhibits Wnt/β-catenin pathway activation in hepatic stellate cell (HSC) (Fan et al., 2023). This evidence concerns the gene FPR1 and Hepatic fibrosis.