Lack of IRF4 in malignant B-cells resulted in faster development of CLL, which was associated with a downregulation of major histocompatibility complex (MHC) molecules on CLL cells and reduced activation of T-cells, suggesting an abrogation of T-cell-mediated leukemia control in these mice [87]. The gene discussed is IRF4; the disease is B-cell chronic lymphocytic leukemia.