Knockdown by shRNA or treatment with either the irreversible tranylcypromine (TCP)-derivative LSD1i or the reversible LSD1i SP2509 disrupted LSD1-binding to CoREST and GFI1/1B, induce differentiation markers (CD86 and CD11b) and morphologic differentiation, repress colony growth, as well as sensitize AML blast progenitor cells (BPCs) to all-trans retinoic acid (ATRA)23,25,29–32. The gene discussed is CD86; the disease is acute myeloid leukemia.