At the core of PNH pathogenesis lies a somatic mutation in the phosphatidylinositol glycan class A (PIGA) gene in hematopoietic stem cells, disrupting GPI-anchor biosynthesis and leading to the absence of complement regulatory proteins such as CD55 and CD59 on the cell surface [1,2]. This evidence concerns the gene PIGA and paroxysmal nocturnal hemoglobinuria.