Under normal conditions, NF-κB is sequestered in the cytoplasm by Iκβ, and oxidative stress caused by hyperglycaemia or other stimuli can activate the Iκβ kinase complex that phosphorylates Iκβ, leading to the activation of NF-κB and inducing the expression of target genes [18]. The gene discussed is NFKB1; the disease is Hyperglycemia.