Moreover, our analyses underline that risk loci in CLL affect genes that participate in interconnecting cellular pathways that are central to B-cell function, including immune response (SP140, BCL6, OAS1, and IRF8)23–26, apoptosis (BCL2L11, CASP8, CFLAR, FAS, BMF, and BCL2)27, and Wnt signaling (UBR5, TLE3, and LEF1)28,29. This evidence concerns the gene LEF1 and B-cell chronic lymphocytic leukemia.