Genetic models that interfere with the utilization of methionine—such as an S-adenosylhomocysteine hydrolase mutant in zebrafish (ducttrip) [17,59] or methionine adenosyltransferase 1A (MAT1A) deficiency in mice [18]—have also been useful in studying NAFLD. This evidence concerns the gene MAT1A and metabolic dysfunction-associated steatotic liver disease.