Recently, PPARα floxed (Pparafl/fl) mice that excise exon 4 to remove all PPARα isoforms were generated and used to develop hepatocyte-specific PPARα KO (PparaHepKO) animals that were shown to have hepatic steatosis on a normal-chow diet [21,22] as well as significantly worsened lipid accumulation, hepatic inflammation, and hyperlipidemia on a high-fat diet [21]. This evidence concerns the gene PPARA and hyperlipidemia.