Upon recruitment to inflamed endothelium via chemokines such as CXCL1 and CXCL8, neutrophils exacerbate vascular inflammation by releasing pro-inflammatory cytokines, including IL-1β, IL-8, and tumor necrosis factor-α (TNF-α), which amplify endothelial dysfunction and promote monocyte adhesion. The gene discussed is IL1B; the disease is endothelial dysfunction.