Using different informatics tools, we recently demonstrated that the majority of the variants that cause severe (<10% of normal G6PD activity, class I and class II) or mild (10–60% of normal G6PD activity, class III) deficiency are primarily located in those functional regions of the enzyme, disturbing the enzyme’s activity and stability25. This evidence concerns the gene G6PD and hyperinsulinemic hypoglycemia, familial, 4.