Mechanistically, METTL3 directly binds to the promoters of the Cd36 and Ccl2 genes and recruits HDAC1/2, which causes deacetylation of H3K9 and H3K27 in their promoters; this, in turn, suppresses the transcription of Cd36 and Ccl2. Furthermore, nuclear METTL3 is decreased in NASH, which is likely owing to CDK9-mediated phosphorylation of METTL3. Here, CDK9 is linked to metabolic dysfunction-associated steatohepatitis.