This study has many limitations: A retrospective design with its use of stored rather than fresh blood samples which may have affected lipid stability in a selective manner, the lack of imaging or biochemical data pertaining to NAFLD status and insulin resistance, and the small number of PNPLA3 148MM genotypes in the normolipidemic group are only but a few. This evidence concerns the gene PNPLA3 and metabolic dysfunction-associated steatotic liver disease.