To further verify the correlation of BMI1 with the malignant myeloid progression and a poor prognosis in patients, especially, to explore the molecular mechanism by which the Bmi1 transfection altered the phenotype of K562 cells, according to Bejar's report, we have firstly analysed the transcription profile of Runx1, Ezh2, Idh2, Pten, Etv6, Cbl, Nras, Asxl1 and Tp53 genes in CD34+ cells of MDS patients by microarray (Fig.4A) [5]. This evidence concerns the gene ETV6 and myelodysplastic syndrome.