Zhou et al. identified that YTHDC2 was significantly repressed in nonalcoholic fatty liver disease (NAFLD) patients, and Ythdc2-depleted hepatocytes led to the accumulation of excessive triglycerides (TGs) by reducing the expression levels of lipogenic genes, including fatty acid synthase, sterol regulatory element-binding protein 1c, and acetyl-CoA carboxylase 1 (Zhou B. et al., 2021). The gene discussed is ACACA; the disease is metabolic dysfunction-associated steatotic liver disease.