The highlights in current study include: A moderate quantity of immune checkpoint CD80 is expressed on the cell surface of FLT3-ITD-positive acute myeloid leukemia; FLT3-ITD augments CD80 expression via an elevated intracellular level of reactive oxygen species (ROS); The HIF-1α inhibitor selectively suppresses the proliferation of FLT3-ITD-positive leukemic cells and triggers CD80 overexpression as a result of excessive ROS generation. This evidence concerns the gene HIF1A and acute myeloid leukemia.