It adequately performs its potential to stimulate a wide variety of cell factors such as cytokines and chemokines leading to more activation of NF-κB. It stops the inflammatory response by overcoming the action of NF-κB from the cytoplasm to the nucleus. Thus, it reduces the cerebral infarction level by impeding necrosis and eventually plays a role as an anti-inflammatory agent. Because of its possible to cross the BBB and prevent Ca2+/calmodulin-dependent phosphodiesterase-1 and voltage-dependent Na+ channels, it has been utilized in ischemic stroke patients. The gene discussed is NFKB1; the disease is cerebral infarction.