Given that miR-181b targeting FPR2 is upregulated in the NAFLD-like experimental animal models and patients with NAFLD, and Fpr2 protein is lower in the CDAHFD-fed female than the chow-fed female mice, it is possible that CDAHFD decreases Fpr2 expression at the post-transcriptional level by increasing miR-181b. Here, FPR2 is linked to metabolic dysfunction-associated steatotic liver disease.