NF-κB expression is enhanced during IR by several mechanisms: HMGB1 signaling via cell surface receptors (Park et al., 2004[57]), increased intercellular Ca2+ concentrations during ischemia that results in the activation of protein kinase C which in turn activates NF-κB (Steffan et al., 1995[74]), stimulation of NADPH oxidase with subsequent ROS production during ischemia (Spencer et al., 2013[73]), and accumulation of mitochondria-derived ROS during IR (Chandel et al., 2000[11]) (Figure 2(Fig. 2)). Here, NFKB1 is linked to ischemia.