It is well known that B-cell receptor (BCR) signaling is important in CLL pathophysiology, resulting in constitutive activation of downstream survival pathways including PI3K/AKT, MEK/ERK or NF-κB pathways, thereby protecting CLL cells from apoptosis, and hence have been exploited as targets for molecular therapies [4, 5]. This evidence concerns the gene NFKB1 and B-cell chronic lymphocytic leukemia.