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The pharmacological activation of  \n           PPAR\u2010<jats:italic>\u03b3<\/jats:italic>  by the thiazolidinediones in diabetes, and of  PPAR\u2010<jats:italic>\u03b1<\/jats:italic> by the fibrates in hyperlipidemia has been shown to help to reduce inflammatory markers in preclinical and clinical studies. PPARs are known to modulate immune pathways through at least three different mechanisms: by direct binding to PPRE of anti\u2010inflammatory cytokines genes; by transrepression of transcription factors like NF\u2010<jats:italic>\u03ba<\/jats:italic>B and AP\u20101; or by corepression. The regulation of the inflammatory pathways by PPARs can be achieved on each one of the cells involved in the atherosclerotic process, that is, monocytes, macrophages, T cells, endothelial cells, and smooth muscle cells. Moreover, as each of these cellular components is interconnected with each other, PPAR activation in one cell type could affect the other ones. 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