PON1 and metabolic syndrome: The overexpression of human PON1 in a LDL−/− mouse model of metabolic syndrome via adenovirus-mediated PON1 gene transfer increased the paraoxonase activity of PON1 4.4-fold and significantly reduced the plaque-associated oxLDL, titer of auto-antibodies against LDL modified by malondialdehyde (MDA) (a proxy for oxLDL), and plaque volume by 80% [65].