Despite these interactions not being confirmed in the context of endogenously expressed proteins, luciferase assays indicated that TCL1 overexpression causes CLL by directly enhancing NF-κB activity and inhibiting AP-1, strengthening the likelihood of effective protein-protein interactions between endogenous proteins and supporting a cross-talk between TCL1 and elements of survival and proliferative pathways. Here, NFKB1 is linked to B-cell chronic lymphocytic leukemia.