The pathogenesis of thrombocytopaenia in malaria is not fully understood but is accepted that encompasses several different mechanisms that lead to increased platelet destruction or consumption, such as increased attachment to endothelium and adherence to Von Willebrand factor, clumping and agglutination of infected and uninfected erythrocytes, consumption into the coagulation process and haemolysis, increased diffuse platelet sequestration, decreased nitric oxide bioavailability, and immune complexes-mediated destruction [23]. The gene discussed is VWF; the disease is malaria.