That endogenous modification of PON1 by lipid dicarbonyls including IsoLG and MDA contributes to reduced PON1 activity observed in vivo during atherosclerosis is supported by our previous observation that IsoLG modification of HDL is enhanced in patients with FH (28) and Ldlr−/− mice and that treating Ldlr−/− mice with dicarbonyl scavengers increased their PON1 activity (26) and reduced atherosclerosis (31). Here, LDLR is linked to familial hyperaldosteronism.