Standard measures are use for the treatment of lymphedema, sensorineural hearing loss, and the other non-malignant anomalies associated with the<unk> . However, treatment of the disorder's myelodysplastic syndrome and acute myeloid leukemia differs somewhat from standard measures. Like other GATA2 insufficiencies,<unk>  is associated with a deficiency of hematological stem and early progenitor cells that is often due to a hereditary loss of one GATA2 gene. Consequently, the use of radical myeloablative conditioning regimens to remove native bone marrow stem/progenitor cells in preparation for hematopoietic stem cell transplantation may entail excessive morbidity and mortality. While no controlled studies on the treatment of the hematological disorders of the syndrome have been reported, current recommendations by multiple authorities suggest the use of hematopoietic stem cell transplantation using non-myeloablative conditioning methods be used when indicated. The use of this procedure should be anticipatory and occur before the development of an excess of progenitor cells populate the bone marrow in cases of myelodyspasia as well as before the development of acute myeloid leukemia. Accordingly, individuals should be routinely monitored by bone marrow examinations and complete blood counts. Furthermore, the relatives of patients afflicted with the syndrome or any of other manifestations of GATA2 deficiency should be tested for GATA2 mutations. Individuals with such mutations are not candidates for donating their stem cells of<unk>  patients. Reversion of the bone marrow to full immune restitution with improved expression of GATA2 can take up to several years after transplantation.
Emberger syndrome
Muir–Torre syndrome
Christianson syndrome
Galloway Mowat syndrome
Mungan syndrome
Fraser syndrome
Zieve's syndrome
Cohen syndrome