NFKB1 and atherosclerosis: Furthermore, our data also demonstrate that SiO2 particles can significantly augment proinflammatory and procoagulant responses through CD40–CD40L-mediated monocyte-endothelial cell interactions via the JNK/NF-κB pathway, suggesting that cooperative interactions between particles, ECs, and monocytes may trigger or exacerbate cardiovascular dysfunction and disease, such as atherosclerosis and thrombosis.