The inflammatory component involves cytokine cascades—particularly Interleukin 1 beta (IL-1β) and Tumor Necrosis Factor alpha (TNF-α)—which exacerbate endothelial dysfunction through the NF-κB-mediated upregulation of adhesion molecules and matrix metalloproteinases [27,28,29,30]. The gene discussed is TNF; the disease is endothelial dysfunction.