Fang et al. showed that shRNA-mediated inhibition of LSD1 in AML cells, contrary to what had been previously described in the normal hematopoietic system, causes a remarkable transcriptional activation of myeloid lineage genes (CD11b/ITGAM and CD86), along with a reduction of AML cell proliferation and clonogenic ability. Here, CD86 is linked to acute myeloid leukemia.