Previous studies have found that lower levels of hemoglobin have been associated with poor outcomes in patients with SAH, including a higher rate of cerebral infarction (Naidech et al. 2006; Naidech et al. 2007; Kramer et al. 2009).This anemia is likely to reflect a suppression of bone marrow activity and response to erythropoietin (Corwin and Krantz 2000; Rodriguez et al. 2001) mediated by increased inflammatory cytokines such as interleukin-1 and tumor necrosis factor associated with SAH (Fink 2004; Gruber et al. 2000; Naredi et al. 2006). The gene discussed is TNF; the disease is anemia.