The increased mortality of AID−/−/Eμ-TCL1 mice with no significant increase in the percentages of CLL cells in the peripheral blood and spleens prompted us to hypothesize that alterations in migration or homing signaling could lead to aberrant trafficking of CLL cells to other organs, resulting in AID−/−/Eμ-TCL1 mice dying earlier than their AID-proficient counterparts. The gene discussed is AICDA; the disease is B-cell chronic lymphocytic leukemia.