Our current and previous studies demonstrate that the deficiency of Ythdc1, Mettl3, or Wtap in the liver leads to liver injury and inflammation,[8, 20] contributing to the pathogenesis of NASH and HCC,[7, 8, 21, 31] indicating that maintaining the expression or activity of YTHDC1, METTL3, and WTAP by small molecules or genetic methods might be an approach to ameliorate liver injury and NASH. This evidence concerns the gene WTAP and metabolic dysfunction-associated steatohepatitis.