The recent article published in Signal Transduction and Targeted Therapy sheds light on the significance of N6-methyladenosine (m6A) methyltransferase-like protein METTL14 in mitigating the progression of metabolic dysfunction-associated fatty liver disease (MAFLD).1 In this study, Wang et al. elucidated the downregulation of METTL14 in hepatocytes from both MAFLD patients and high-fat diet (HFD)-induced MAFLD mouse models, underscoring its pivotal role in maintaining hepatic lipid and redox homeostasis in normal livers. This evidence concerns the gene METTL14 and fatty liver disease.