Malaria has exhibited the strongest known selective pressure on the human genome observed in recent history and has been proven to be the driving force behind a variety of human polymorphisms associated with malarial disease outcomes and severity, such as the sickle-cell trait, thalassaemia, glucose-6-phosphatase deficiency (G6PD), and other erythrocyte variations6,7. This evidence concerns the gene G6PD and hyperinsulinemic hypoglycemia, familial, 4.