Severe malarial infection is associated with the rupture of parasitized red bloodcells releasing malaria pigment and other soluble antigens and toxins that stimulatethe overproduction of TNF-α in human monocytes and may also stimulate intense Thelper type 1-like response locally, in tissues of vital organs which result inupregulation of expression of endothelial adhesion molecules such as intracellularadhesion molecule-1 (ICAM-1) or other adhesion molecules. This evidence concerns the gene TNF and malaria.