Given the high prevalence of glucose 6-phosphate dehydrogenase (G6PD) deficiency (up to 30%) in sub-Saharan Africa [44], and the fact that G6PD deficient children are prone to the haemolytic effect of the oxidant metabolite of dapsone [45], halting the development of ACD for malaria treatment in Africa was justified. This evidence concerns the gene G6PD and G6PD deficiency.