Adherence of sickle RBC stimulates endothelial cells to upregulate their adhesion molecules, which accelerates the adhesion cascade.1 Activated endothelium also releases a broad range of cytokines, including granulocyte-macrophage-colony-stimulating factor (GM-CSF), interleukin (IL)-1, IL-3, IL-6, IL-8 and tumor necrosis factor (TNF-a), and these have been detected in the plasma of patients with SCD.2,3 Neutrophils may also become activated during this cascade of vasoocclusive events, and neutrophil adherence may contribute to vasoocclusion,3 as well as endothelial cell damage.4 This evidence concerns the gene TNF and Schnyder corneal dystrophy.