Therefore, combined the results of this study, we speculated that the mechanism of Fmnl1 participating in NASH fibrosis might be that the increased expression of Fmnl1 facilitated the differentiation of monocytes to macrophages and the dynamic changes of podosomes, promoted the release of pro-fibrogenic cytokines and activated HSCs, thereby promoted the production of liver collagen in NASH. This evidence concerns the gene FMNL1 and metabolic dysfunction-associated steatohepatitis.