Chronic exposure to cytokines including IL-1β, IL-6, TNF-α, and C-reactive protein (CRP) promotes endothelial dysfunction with increased expression of surface adhesion molecules (VCAM-1, ICAM-1, and selectins),116 facilitating leukocyte adhesion, activation, and neutrophil extracellular trap formation (NETosis, the release of chromatin nets that can trigger thrombosis).117. This evidence concerns the gene CRP and endothelial dysfunction.