PIGA and paroxysmal nocturnal hemoglobinuria: One of the most frequently reported somatic mutations, found in nearly half of AA patients, is PIGA, which results in clonal populations of cells lacking cell surface proteins linked to a glycosylphosphatidylinositol (GPI) anchor due to somatic loss-of-function mutations, one of a number of drivers of clonal evolution in AA and paroxysmal nocturnal hemoglobinuria (PNH) [100–102].