There are several lines of evidence supporting TNF's role in SAH: (i) cerebrospinal TNF levels rise and peak 4–10 days post-SAH ictus (293–295), the timeframe when delayed autoregulatory disruption and ischemia generally occurs; (ii) TNF levels associate with perturbed cerebral flow velocities and poor outcomes (293, 296, 297); and (iii) anti-TNF therapy (i.e., etanercept or adalimumab) reduces vascular constriction and/or neurological injury in experimental SAH (298–300). This evidence concerns the gene TNF and ischemia.