In the second case, we speculate that higher PON1 was not protective in HR1 stemming in one way or another from the inadequacy of PON1 to significantly inhibit oxidation of the presumably heavier load of small dense LDL particles very likely present in this population enriched with Metabolic Syndrome subjects (Table 1; HR1—51.3%, HR2—9.7%, p < 0.001). This evidence concerns the gene PON1 and metabolic syndrome.