While complexes containing the RelA subunit, inducing transcription of a panel of pro-apoptotic genes, are mainly responsible for the stroke-triggered neurodegeneration [20, 35], activated c-Rel-containing NF-κB dimers participate in anti-apoptotic gene regulation and counteract ischemic damage by acting as an innate neuroprotective mechanism [36]. The gene discussed is REL; the disease is Stroke.