Functionally, MDSCs isolated from the bone marrow of OPN5-treated mice were less capable of suppressing T-cell proliferation and demonstrate that the effects of OPN5 on MDSC activity are maintained in vivo, highlighting the therapeutic potential of BRD4 targeting in re-programming MDSCs to enhance immune-mediated tumor control in CLL. The gene discussed is OPN5; the disease is B-cell chronic lymphocytic leukemia.