Indeed, they found that susceptibility to complement‐mediated lysis of erythrocytes from PNH patients may be severe (15–25 times the normal one), or just a moderate (3–5 times the normal one),35, 36 eventually prompting the subsequent identification by flow cytometry of possible complete or partial deficiency of GPI‐linked proteins (referred as type III and type II PNH phenotypes, respectively),37, 38 which may result from null and non‐null PIGA mutations.39 This evidence concerns the gene PIGA and paroxysmal nocturnal hemoglobinuria.