As shown in Table 2, there is a significant interaction between the presence of ≥1 hyperapoB variants, in either the LPL, APOE, or PPARα genes, and smoking habits on the risk to exhibit apoB > 0.9 g/L, but only among subjects with a low risk profile, that is without MetS and with LDL-C < 3.5 mmol/L. This evidence concerns the gene APOE and metabolic syndrome.