The genetic lesions that underlie CLL are heterogeneous and include copy number alterations and point mutations in over 200 putative CLL driver genes that cluster into several distinct biological pathways, including cell cycle regulation, DNA damage response, RNA processing, chromatin modification, and BCR, WNT, NOTCH and NF-kB signaling [5, 6]. Here, NFKB1 is linked to B-cell chronic lymphocytic leukemia.