The exact pathogenesis of NAFLD is not clarified completely, but increasing evidence supported the role of single nucleotide polymorphism (SNP) in the risk and development of NAFLD, especially SNPs within those genes associated with lipid handling and oxidative stress, such as the patatin-like phospholipase domain containing protein 3 (PNPLA3), glucokinase regulatory protein gene (GCKR), and apolipoprotein C3 (APOC3) gene [5, 6]. This evidence concerns the gene PNPLA3 and metabolic dysfunction-associated steatotic liver disease.