Proposed model of the effect of ectopically expressed SNAI1 on normal hematopoiesis and LSD1 function. During normal hematopoiesis, balanced myeloid development is observed, resulting in normal numbers of mature myeloid cells. Ectopic SNAI1 in hematopoietic cells interacts with LSD1 and subsequently leads to inhibition promotion of myeloid differentiation along the granulocyte and macrophage lineages. This complex drives expanded myeloid cell differentiation and production of excessive numbers of mature myeloid cells, resulting in myeloproliferative phenotypes. SNAI1/LSD1 complex also imbues enhanced self-renewal capacity on immature myeloid cells, allowing these cells to expand and potentially accumulate additional mutations that can result in AML development over an extended period of time. We propose that the interaction between SNAI1 and LSD1 drives myeloid developmental defects through physical interaction at SNAI1 gene targets containing the canonical E-box motif and subsequent modulation of LSD1 function and inhibition of LSD1 binding to its normal hematopoietic transcription factor partners, such as GATA1/2, SALL4, and GFI1/1b, and subsequently compromising the function of these key hematopoietic transcription factors.