In contrast, autosomal recessive p47-phox deficiency (25% of all CGD cases [19], [20]) is mostly due to recombination events between the NCF1 gene and one out of two highly homologous pseudogenes, thus leading to the same GT deletion at the beginning of exon 2 in 80–90% of all p47-phox–deficient CGD patients. The gene discussed is NCF1; the disease is hyperinsulinemic hypoglycemia, familial, 4.