Activation of TGF-β signaling as a resistance mechanism is supported by our previous data that demonstrated a potential role of TGF-β signaling in modulating the sensitivity of AML cells to chemotherapeutic agents, in which the blockade of TGF-β1 enhanced the response to the combination of cytarabine and CXCR4 inhibitor (plerixafor) in vitro and prolonged survival in an in vivo leukemia model [42]. The gene discussed is TGFB1; the disease is acute myeloid leukemia.