Acute myeloid leukemia (AML) is a heterogenous disease with multiple morphological, immunophenotypic and genetic features. The t(8;21), which results in the expression of RUNX1-ETO (aka AML1-ETO), is accountable for 12% of AML cases (1). Previously, this fusion protein has been shown to block hematopoietic development of normal human hematopoietic stem and progenitor cells (HSPC), as well as promoting the cells’ self-renewal potential (2,3). Even though several studies have determined the transcriptomic changes observed in cells expressing RUNX1-ETO, there is a paucity of studies quantitating proteomic changes. Given that transcriptional regulation is likely mediated by changes in transcription factor (TF) expression, I hypothesize that RUNX1-ETO leads to TF dysregulation, of which critical components might dictate differentiation blockage.