Sickle cell disease (SCD) is characterized by malformed erythrocytes and results in many vascular complications, including the lysis of a minor proportion of these cells, liberating free hemoglobin, which is a potent scavenger of nitric oxide (NO). SCD involves inflammatory activation, including the upregulation of vascular coagulation. Because NO possesses important anti-coagulant and anti-adhesion properties, the increased scavenging of NO in SCD undoubtedly is a major contributor to the pathology of this disease.