Further investigation of these regulatory mechanisms in CGD will be greatly facilitated by the development of an in vitro model based on iPSC carrying mutations in all NADPH oxidase subunits, particularly since activation of the enzyme relies upon cytosolic phosphorylation of a p47phox–p67phox dimer to potentiate its binding to the gp91phox and p22phox subunits located in the cytoplasmic membrane. This evidence concerns the gene NCF1 and chronic granulomatous disease.