In adult falciparum malaria, there is also decreased endothelial and pulmonary NO bioavailability associated with low levels of the NOS substrate L-arginine [6], increased levels of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) [10], NO quenching by cell-free hemoglobin [11] and L-arginine reversible endothelial dysfunction in moderately severe malaria [6]. This evidence concerns the gene NOS2 and malaria.