These data suggest that fatty acid β-oxidation, lipogenesis, and VLDL secretion do not contribute to the increased liver steatosis seen in Mettl3-HKO mice and suggest that increased CD36-mediated hepatic free fatty-acid uptake leads to more severe NALF and NASH in Mettl3-HKO mice. The gene discussed is METTL3; the disease is metabolic dysfunction-associated steatohepatitis.