Importantly, due to the complexity of lipid metabolism and the mechanisms of gene-environment interactions in metabolic diseases, previous studies found that the genetic variants with the greatest impact on RC concentrations were found at a key point of lipoprotein metabolisms, such as apolipoprotein E (APOE), apolipoprotein C3 (APOC3), and apolipoprotein C2 (APOC2) genes encoding apolipoproteins and genes encoding enzymes involved in residue degradation, such as lipoprotein lipase (LPL) (1). This evidence concerns the gene APOC3 and metabolic disease.