As hypothesized, there was an over-expression of genes encoding: anti-fibrinolytic agent, cellular adhesion molecules, cytokines/chemokines, growth factors and caspase 1, which cleaves pro-IL-1 and pro-IL-18 in their active forms [79]; and finally TLRs, which are stimulated by FFA and involved in atherosclerosis [37], and molecules involved in TLR and IL-1 signaling: MyD88, NF-κB and iNOS. Here, IL1B is linked to atherosclerosis.