Mettl3 transcript abundance was increased in the macrophages from obese mouse livers and myeloid-specific Mettl3-knockout resulted in inhibited HFD-induced obesity in mice with lower hepatic lipid accumulation, inflammation, and fibrosis, demonstrating m6A involvement in immune mechanisms that contribute to NAFLD and progression to NASH [164]. The gene discussed is METTL3; the disease is metabolic dysfunction-associated steatotic liver disease.