For instance, PPARγ activation is demonstrated to suppress inflammation via inhibiting NF-κB signaling pathway and decrease lipid accumulation via enhancing RCT through upregulation of LXRs–ABCA1/G1 signaling pathways; while PPARγ inactivation is indicated to decrease lipogenesis and CD36-mediated lipid uptake, thereby suppressing lipid accumulation and hyperlipidemia-induced inflammation. This evidence concerns the gene PPARG and hyperlipidemia.