Although PPARα activation by fibrates decreases ApoB-containing lipoproteins as well as total serum ApoB levels in rodents and human (Peters et al., 1997; Milosavljevic et al., 2001), treatment of Ldlr−/− mice with ciprofibrate markedly decreased plasma ApoB-48-carrying IDL and LDL but at the same time caused a marked accumulation of ApoB-100 carrying IDL/LDL, increased plasma cholesterol levels and promoted aortic atherosclerosis (Fu et al., 2004). This evidence concerns the gene APOB and aortic atherosclerosis.