As HO-1 has been noted to drive proliferative signaling resulting in resistance to chemotherapeutic agents in myelodysplastic syndrome [23], we used an isogenic pair of TKI-sensitive (ITD) and -resistant (ITDR) FLT3-ITD-expressing BaF3 cells to determine if HO-1 was also basally altered in TKI-resistant AML populations. This evidence concerns the gene FLT3 and myelodysplastic syndrome.