As NF-κB is activated and enters the nucleus, it regulates the transcription of the pro-inflammatory mediators cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), which promote endothelial cell inflammation and apoptosis, invoking endothelial dysfunction and diabetic vascular complications [5,6]. The gene discussed is NFKB1; the disease is endothelial dysfunction.