During cerebral ischemia, the activated NF-κB dimers are subsequently translocated into the nucleus where they selectively bind to specific DNA sequences called κB sites; promoter domains present a large number of proinflammatory genes and subsequently cause TNF-α, IL-1β, IL-6, ICAM-1, PGE2, COX-2, and iNOS translation [6, 105, 106]. The gene discussed is NFKB1; the disease is brain ischemia.