It has been reported that dysregulated mir-21 was essentially implicated in endothelial dysfunction, progression of early to advance atherosclerotic plaque, formation of critical coronary stenosis, and thrombus leading to acute coronary syndrome through activation of different inflammatory cells, cytokines, and signaling pathways including macrophages, tumor necrosis factor-α (TNF-α), interleukin- (IL-) 17A, IL-1β, IL-6, phosphatase and tensin homolog (PTEN), PI3K/Akt MAPK, vascular endothelial growth factor, and TLR4/NF-κB [5–9]. Here, NFKB1 is linked to endothelial dysfunction.