Indeed, for PNH a dual pathophysiology has been postulated: (a) the occurrence of a somatic mutation in the phosphatidylinositol N‐acetylglucosaminyltransferase subunit A (PIGA) gene in one or more hematopoietic stem cells (HSCs)4, 5, 6; and (b) the clonal expansion of these PIGA‐mutated HSCs, due to an immune escape from the T‐cell mediated autoimmune attack destroying normal (PIGA‐unmutated) hematopoietic progenitors.7, 8, 9. This evidence concerns the gene PIGA and paroxysmal nocturnal hemoglobinuria.