On the other hand, endothelial dysfunction also stimulated the proinflammatory cytokine secretion, such as IL-1Beta, IL-6, IL-8, and TNF, and activated several signaling pathways that include PI3K, Akt, and MAPK that could activate the Nf-kB as a transcription factors inducing inflammation and extracellular matrix secretion as a mediator of macrophage attachment (Figure 1) [26]. The gene discussed is NFKB1; the disease is endothelial dysfunction.