Recently, impaired IFN signaling in CLL B cells (loss of IFN regulatory factor 4, IRF4 using a murine model or its reduced expression in human CLL cells) has been linked to downregulated antigen presentation and co-stimulatory molecules that prevented the generation of activated, exhausted T cell responses and was associated with accelerated disease progression. This evidence concerns the gene IFNA1 and B-cell chronic lymphocytic leukemia.