In contrast, Li and colleagues found that hepatocyte-specific deletion of METTL3 promoted NAFL-to-NASH progression by enhancing CD36-mediated hepatic-free FA uptake and CCL2-induced inflammation, whereas hepatic upregulation of METTL3 protected against NASH progression by suppressing the expression of CD36 and CCL2. Here, METTL3 is linked to non-alcoholic fatty liver.