mmLDL induces rapid, JNK-dependent phosphorylation of Jun, which leads to removal of NCoR and derepression of AP-1. This, together with rapid phosphorylation of ERK1/2, results in the completion of the AP-1 transcription complex, which is later strengthened by delayed ERK1/2 and Jun phosphorylation induced by LPS 111. However, LPS-induced Jun phosphorylation is mediated by IKKε, which is brought to the promoter region with the NF-κB transcription factors 127. Cooperative activation of AP-1 and NF-κB result in increased expression of proinflammatory genes induced by co-stimulation with mmLDL and LPS 111.