progenitors are leukemic, and not the granulocyte precursors. In this form of AML, levels of erythroblasts can reach up to 94.8% of all nucleated cells in the bone marrow, and the immature forms of the erythroblasts, the proerythroblasts and basophilic erythroblasts, are more commonly found. One study noted that in control leukemic groups with general AML, immature erythroblasts accounted for 8% of all erythroid cells, but in a group with pure erythroid leukemia, this number was a minimum of 40%, and ranged up to 83%. Furthermore, in the case of pure erythroid leukemia, the immature erythrocytes are most morphologically affected, being larger and sometimes bi- or tri-nucleic. Hence the most affected stages of erythrocyte development in pure erythroid leukemia are the same stages in which HOXA9 expression is greatest. Interactions HOXA9 has been shown to interact with: MEIS1, PBX2, and TRIP6. HOXA9 expression is regulated by several genes, including UTX, WHSC1, MLL and MEN1. UTX, MLL and WHSC1 code for protein methylation and demethylation activity, specifically for the histone methyltransferase complex, of which increased levels have been shown to correlate with higher HOXA9 expression. MEN1 codes for the tumour suppressing protein menin, and lower menin levels as a result of MEN1 excision correlate with low HOXA9 expression. UTX and WHSC1 also display similar expression patterns to HOXA9, being lowest in the embryonic erythrocyte lineage, higher in the fetal stage and showing highest expression in the adult stage. MLL and MEN1, however, show consistent expression through each erythroid lineage, and it is possible that some other transcription factor may be interfering with the actions of these genes on HOXA9 during the embryonic stage. HOXA9 itself regulates a vast array of genes, such as Flt3, Erg, Myb and Lmo2, all of which exhibit the characteristic increasing expression pattern through the erythroid lineages displayed by HOXA9. Furthermore, mutations in each of these genes have been implicated in cancers. Flt3 duplication is observed in 20% of AML cases, and along with NUP98 translocation, it is associated with a poor prognosis. Erg and Myb are part of two families of transcription factors which, when mutated, correlate strongly with prostate cancer and myeloblastosis respectively. Lmo2 is associated with T-cell leukemias, and is also essential to erythropoiesis in early developmental stages, as Lmo2 knockout mice experience yolk sac erythropoiesis failure and the embryo dies around 10.5 days post coitus. This seems to contradict with the observed expression