NFKB1 and isolated hemihyperplasia: In an IH animal model, p38 MAPK levels were significantly increased, which could activate the NF-κB signaling pathway, releasing cytokines such as IL-1 β, IL-6, and TNF-α, oxidative species, and adhesion molecules.523 The release of cytokines, in turn, promotes the production of ROS by microglia, thereby perpetuating inflammation and aggravating ongoing oxidative stress.524,525 CNS neuronal damage and apoptosis from IH might involve other mechanisms.