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We also consider how the course of the disease and the response to immuno\u2010suppressive therapy are influenced by the nature and specificity of the pathogenic process. A somatic mutation of the<jats:italic><jats:styled-content style=\"fixed-case\">PIGA<\/jats:styled-content><\/jats:italic>gene underlies the clonal disease paroxysmal nocturnal haemoglobinuria (<jats:styled-content style=\"fixed-case\">PNH<\/jats:styled-content>): there is direct evidence that the expansion of the<jats:italic><jats:styled-content style=\"fixed-case\">PIGA<\/jats:styled-content><\/jats:italic>mutant clone results from Darwinian selection exerted by a glycosyl\u2010phosphatidyl\u2010inositol \u2010specific auto\u2010immune attack. Thus,<jats:styled-content style=\"fixed-case\">PNH<\/jats:styled-content>patients are a unique subset of patients with<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>, in whom haematopoiesis recovers through this escape mechanism. A similar process, although less effective, may operate when the auto\u2010immune attack is against a human leucocyte antigen (<jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content>) molecule and an<jats:italic><jats:styled-content style=\"fixed-case\">HLA<\/jats:styled-content><\/jats:italic>mutation has produced a clone missing that molecule. We then discuss the significance of other mutant clones that are frequently found in<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>, presumably due to a combination of genetic drift and selection. These clones are not causative of<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>, but they emerge in<jats:styled-content style=\"fixed-case\">AA<\/jats:styled-content>and they may be pre\u2010leukaemic: unlike a<jats:italic><jats:styled-content style=\"fixed-case\">PIGA<\/jats:styled-content><\/jats:italic>mutant clone, in general they are unable to effectively reconstitute haematopoiesis.<\/jats:p>","DOI":"10.1111\/bjh.15443","type":"journal-article","created":{"date-parts":[[2018,7,5]],"date-time":"2018-07-05T12:08:51Z","timestamp":1530792531000},"page":"758-776","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":111,"title":["Advances in understanding the pathogenesis of acquired aplastic anaemia"],"prefix":"10.1111","volume":"182","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4663-8790","authenticated-orcid":false,"given":"Lucio","family":"Luzzatto","sequence":"first","affiliation":[{"name":"Muhimbili 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