Several mechanisms are involved in NF-κB pathway activation, such as hyperglycemia-induced IKKβ overexpression, increased Protein kinase C (PKC) activity, and the formation of advanced glycosylation end products (AGEs), which bind to specific receptors, i.e., receptors for advanced glycosylation end products (RAGE) on vascular smooth muscle cells, leading to oxidant stress, i.e., reactive oxygen species (ROS), and increased adhesion molecules, such as ICAM-1 and vascular cell adhesion molecule-1 (VCAM-1). Here, IKBKB is linked to Hyperglycemia.