Our results showing the similarities of the HCDR3 expressed by the expanded Traf2DNxBCL2-tg+/+ CLL/SLL clones to those recognizing autoantigens and pathogens suggest that antigen-stimulation would also drive disease progression in our CLL/SLL mouse model, similarly to what has been demonstrated in the Eμ-TCL-1-tg mice (31, 51). The gene discussed is TG; the disease is B-cell chronic lymphocytic leukemia.