A growing body of evidence suggests that upon activation of NF-κB/P65, the pro-inflammatory response was associated with ROS which leads to endothelial dysfunction; thereby, a dozen amounts of cytokines and chemokines such as IL-1β, tumor necrosis factor-alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) are activated, which adds to the escalation of inflammation [28]. The gene discussed is CCL2; the disease is endothelial dysfunction.