The authors proposed inhibition of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) as one mechanism of cardioprotective actions following pretreatment with PPARα and/or γ agonists, as they observed an increase of NF-κB pro-inflammatory target genes such as monocyte chemoattractant protein-1 (MCP-1) and inducible nitric oxide synthase (iNOS) after myocardial infarction, whose expression was attenuated in case of pretreatment with 15D-PGJ2. The gene discussed is CCL2; the disease is myocardial infarction.