a range of 18 to 95 months. an nih intervention study is in the process of recruiting and treating 144 individuals with gata2 deficiency to determine the success of a treatment regimen consisting of medication (fludarabine, busulfan, cyclophosphamide) and total body irradiation conditioning followed by allogenic hematopoietic stem cell transplantation. prognosis overall survival in a nih study using a modest conditioning regimen followed by hematologic stem cell transplantation in gata2 deficient patients affected by immune deficiencies was 54% at 4 years; gata2 deficient children transplanted for mds with monosomy 7 experienced a 5-year survival of 68%. history in 2011, all cases of the previously described disorders of emberger syndrome and monomac as well as some cases of the previously described disorder of familial mds/aml were discovered to be due to inactivating mutations in the gata2 gene. subsequently, numerous studies discovered that a significant percentage of many other well-known hematological, immunological, autoimmune, and infectious diseases were associated with, and apparently due to, inactivating mutations in the gata2 gene.