In our studies of in vivo, we found that a ~10-fold in NCD-feeding mice, or a ~15-fold in HCD-feeding and ob/ob mice (Figs 3a and 4a) increase of hepatic miR-27a were efficient enough to repress hepatic Fas and Scd1 expression and therefore alleviate NAFLD. Here, FAS is linked to metabolic dysfunction-associated steatotic liver disease.