The fact that only the Traf2DNxBCL2-tg+/+ mice develop CLL/SLL highlights the need of both Traf2 deficiency and BCL2 overexpression for promoting CLL development in this mouse model and underlines a role for autoantigens- and pathogen antigens-specific HCDR3 in driving disease progression. This evidence concerns the gene TRAF2 and B-cell chronic lymphocytic leukemia.