NF-κB can be activated by a wide array of exogenous and endogenous stimuli including hyperglycemia, elevated free fatty acids, ROS, TNF-α, IL-1β, and other pro-inflammatory cytokines, advanced glycosylation end-product-binding and receptor for AGE, p38 MAPK, DNA damage, viral infection, and ultraviolet irradiation (Barnes and Karin 1997). Here, NFKB1 is linked to Hyperglycemia.