The human ERYF1 gene (summary) NF-E1 DNA-binding protein GATA1, locus Xp11.23 [§§; †] containing 2 'finger' motifs referred to as ERYF1 of an erythroid-specific gene. The cDNA for the human ERYF1 gene is almost identical to that of chicken and mouse GATA1 gene consisting of 2 zinc finger' type motifs its activator domain contains the binding sites for protein GATA1 and the CACCC (HS2)^ region. FOG is specific to this complex corresponding cDNA and interacts with element in the beta-globin IVS2 promoter from hemoglobin protein subunit promoters (alpha-chain gene‡, gamma, epsilon^ and (embryonic), a switch from fetal to adult haemoglobin -or- relative to the T to C substitution of fetal hemoglobin (HPFH), implications for fetal hemoglobin - HbF``) distinct for erythroid (INHBA) and megakaryocyte differentiation, in vertabrate though, the N- and C-terminal thirds of the human protein. Friend of GATA-1, FOG1; ZFPM1, zinc finger protein region a coregulator of the GATA1 associations facilitates a chromatin locus control region-(LCR) modifying proximity fetal to adult (gamma) to beta globin including the erythroid (EKLF krüpple-like) factor DNAse1^ histone hypersensative site (HS)^ locus (LCR) GATA1 establishes, facilitates interactions with immunoprecipitation, cross-regulatory roles reduced histone, acetylation and antagonism (EKLF-FlI-1) mechanisms. PU.1 - of the Ets family is 'synergistic' to the major basic protein, (MBP) handles bistability in the erythroid-'myeloid switch « directed by PU.1,' influenced DNA binding and is involved with MZF-1 (myeloid zinc finger 1), it interacts with the 'C-terminal zinc finger « (CF)' of GATA1. A bipotential function in multiple contexts (erythroid versus megakaryocytic myeloid cells, GATA1 switches myeloid cell fate into eosinophils)° as two multi-protein complexes when segregated into two types (factor P-TEFb) one of the characteristics of (TAL-1, T-cell acute-) leukemic (SCL) stem cells is both types in circulating blood, for both the downregulation of GATA-1 and with the upregulation of GATA-2 (3q21)° that CD34␠ has the transcription capacity observed in immature hematopoietic progenitor stem cells, specific regions of each (Sequencing of FOG1 with GATA1 and GATA2), requires intact DNA-binding domains. The C-terminal zinc finger (CF) basic tail shares, in an antagonistic fashion 'mutations' in exon 2‡ (-GATA1s is a shorter GATA1 isoform (sf) found in DS (Down syndrome) a transient leukemia (TL)-AMKL) that lacks the transactivation'" domain, in cis-acting GATA element, identification requires intact long forms (lf) of NF-E1 DNA-binding domain. Two novel zinc-finger domains demonstrate that the NFE1 gene cDNA-binding protein is assigned the human locus located in Xp11.23, required for normal megakaryocytic and erythroid development. A mutation in the FOG1-GATA1 N-terminal zinc finger (N-finger of leukemic cell (Igs)-immunoglobulins) or lacking the N-terminal activation the binding of Fog1 and the N-finger in the DNA face of Fog1, with non X-linked associations (16q22-24) if different clinical entities linking to X-linked (X is any amino acid, substitution in the DNA-binding (Nf) region) thrombocytopenia in males-(XLTT*'-GATA1) with anemia low platelet levels traces discernable steps as embryos with a defect in forming erythroid burst-forming units BFU-E ☞ (summary - of all DNA that is transcribed which occurred at a exome splice site), to Minimal residual disease MRD - (cancer, "preleukemia" - myeloproliferative disorder (TMD), myeloid leukaemia-AML, SCL° and megakaryocytic AMKL) the GATA1-HS2-modified vector allowed remission in blood component and heme (Protoporphyrinogen) at the seventh GATA site in exon 1*'/intron-7° as a cofactor involving 6 non-coding exons and transactivation by USF1 and GATA1. A DNA Cytosine mechanism ara-c (Arabinofuranosylcytosine) short (sf) and (lf) long forms is used to kill these megakaryocytic cancer cells; clarifies that GATA-1 controls genes that manipulate the cell cycle and apoptotic cell death underlying normal (PI3K) and pathologic (PU.1) erythropoiesis - 'differentiation' is (FKBP12) lacking basal expression'" in contrast to Bcl when Bcl-X(L) is cleaved by caspases. Anti-apoptotic Hsp70 protects GATA-1 during the switchingª of the erythroleukemia␠ cells that fail to complete maturation, proteolysis undergoing cell death in both the megakaryocytic and erythroid cells, established that phospholipase C (PLC)ª is involved in the signalling pathway (PI3K)/Akt equally expressed 'as' a probable negative FOG regulator, interacts with the PU.1 related Ets domain of glycoprotein (GP)(1) VI*' by expressing thrombopoietin activation of platelets in megakaryocytic cell lines, expressing both Fli-1 and GATA-1. A weak loss of aspartate in the amino-N-terminal zinc finger (Nf) loop GATA1's three base substitution mutations results in incomplete megakaryocyte/platelet maturation as assessed by the DNA demethylating agent 5-azacytidine, activity in the presence of ara-c which occurred at a exome splice site. GATA1 appears to interact with RNA-mediated basal expression against these pathways, associated protein or mammalian targets clarified that the basal transcription apparatus with transcription factors`` appears to interact with an HS2 region mutated in its GATA motif -GATA1s a shorter GATA1 isoform.