Recently, the SP2509 LSD1 inhibitor has been demonstrated to impact on JAK/STAT3 signaling [56] as well as pro-survival protein expression/stability of BCL2 and MCL1 respectively [57] and may explain why the SP2509 inhibitor is more active in ETP-ALL than the GSK-LSD1 compound. The gene discussed is STAT3; the disease is acute lymphoblastic leukemia.