Model for KLF regulation of the activity of NF-κB in the presence of APLA/anti-β₂GPI antibodies. CBP/p300 regulates the activation of endothelial cells because it is an essential cofactor for NF-κB and the KLFs. A dynamic equilibrium exists between binding of CBP/p300 to the KLFs and NF-κB. The decrease in KLF levels that occur during APLA/anti-β₂GPI–induced endothelial cell activation allows the preferential association of CBP/p300 with NF-κB, thus promoting the transcription of NF-κB–dependent genes, such as cell surface adhesion molecules (E-selectin) and tissue factor.